Tenaya Therapeutics, Inc. (TNYA) Earnings Call Transcript & Summary

Okay. Great. Good afternoon, everyone, and thanks for joining us at the Morgan Stanley Global Healthcare Conference. I'm Michael Ulz, one of the biotech analysts here. And it's my pleasure to introduce Faraz Ali, CEO of Tenaya Therapeutics. Before we get started, I just need to read a quick disclosure. For important disclosures, please see the Morgan Stanley research disclosure website at www.morganstanley.com/researchdisclosures. And if you have any questions, please reach out to your Morgan Stanley sales representative. And with that, Faraz, thanks for joining us today, and I'll -- maybe I'll hand it over to you, and you can give us some just introductory comments for people that may not be familiar...

Yes. Just overall, before we dive into the deeper questions, I just wanted to say that we've had a great start to the year and looking forward to closing strong. Everything that we set out do in our guidance, we've accomplished. So on our 201 lead gene therapy program for the leading genetic cause of HCM, we dosed -- successfully dosed the high-dose cohort, successfully got the DSMB clearance, which is important from a safety perspective. We've released data from our natural history study, which is the largest natural history study in the world for this disease for the children with this mutation, a very severe disease. And then we're on track to deliver data in the second half of this year, and we had first narrowed our guidance to Q4, but we're happy to share today breaking news at Morgan Stanley Healthcare Conference that as of 2:00 p.m. Eastern today, we're able to share that we were accepted for a late-breaker clinical presentation in the main conference at the American Heart Association. Happens to be a joint session of the American Heart Association and the Hypertrophic Cardiomyopathy Society. So it's a big event for us in general this year and even bigger now that we'll be giving our data update in November now. So we're able to announce that. That was not shared before. And then on 401, DITTO hitting all of our milestones. We dosed the first dose cohort successfully. We got DSMB clearance. We've already started dosing in the high-dose cohort. So that's already announced. Also presented data from the largest natural history study in the world for that condition. 190 patients have been enrolled in that natural history study, and we're on track for delivering data in Q4. No big announcements there. But presumably, that data will be released around the same time as the AHA presentation for 201. So we have met all the objectives that we set out for this year so far, and we're closing in on the most important stuff, which is delivering data -- meaningful data updates in the second half in Q4.

Great. Thanks for that introduction. Also congratulations on the late-breaker at AHA, very exciting. And I thought maybe we can just start with a couple of big picture questions, gene therapy, FDA, sort of what's happening there and maybe just any thoughts you have there that you want to share.

Yes. I mean, first, I want to say, and I have a fellow -- I sit on the -- so I sit on the Board of Alliance for Regenerative Medicine. I have a fellow Board member in the audience here. And one thing I will speak both as a Tenaya CEO, but also as a Board member of the Alliance for Regenerative Medicine, which is the largest industry organization for the cell and gene therapy field, we should stop thinking about like the FDA as like individuals or like Democratic leadership or Republican leadership. From our vantage point, the FDA -- their commitment to rare diseases, their commitment to cell and gene therapy for rare diseases and cell and gene therapy in general, it's a bipartisan support that we see. So when we have gone to Washington, D.C., when we've seen the roundtables that they've held, there is a consistent commitment for innovative medicines for rare diseases. They recently released some new sort of pathways for diseases that might be relevant to some of us in the field. So overall, I feel that the FDA, yes, there have been some comings and goings of some people. And -- but overall, I think that the environment is as positive as it's ever been, even though there have been changes in leadership over there. And then the other thing I would say about the FDA, the main thing that we all worry about is, are they going to keep to the alignments that they've already announced, right? And that's really important to us because some of those alignments are with peer companies, Rocket, Lexeo, ReGenX, uniQure, where they've said, yes, you can pursue accelerated approval based on protein plus some other surrogate marker for an accelerated approval. And the big concern is, are they going to change their stance? Was that just a feature of Peter Marks and Nicole Verdun? And from both private -- discussions with individuals plus their own public statements, we see no changes in the stance of the commitment to accelerated approval pathways based on surrogate markers, including protein. And so that's a positive. So overall, yes, a lot of drama maybe at the FDA, but the substance remains the same and it remains positive. And I will continue to say, I think it's as positive a time as it's ever been for cell and gene therapies for rare diseases.

Got it. That's good to hear. And I guess maybe another sort of topical question just in gene therapy space just has to do with the immunosuppressive regimens. And maybe you can share your thoughts on some of the changes that are being going on out there in sort of how that influences your program and what's your regimen look like?

I mean we all put patients first. And so their safety is paramount. We -- I think I'm not alone. I think we all -- all of us are thinking about that every day. It's terrible what happened. In the last couple of months, we had both a death in the Rocket's study for Danon disease as well as 3 deaths in the Sarepta's study or -- well, commercial products, so 2 DMD and 1 limb-girdle. So 4 in total deaths have happened in short order. And I think it's important to first understand what it was and what it wasn't. What it was is in the case of Rocket, they said, and the FDA agreed the death was attributed to the use of a -- an experimental use of a C3 inhibitor to blunt complement activation in those patients. And they had not seen that before, the kind of capillary leak syndrome with their established regimen in prior patients. They only saw it here. They discontinued it. And no read-through to us. We're not using that C3 inhibitor or any other prophylactic complement inhibitor. And in the case of Sarepta, I think that was an instance where they may not have been doing enough on the immune suppression side. They were only giving corticosteroids. And in limb-girdle and in DMD, corticosteroids is like the foundational standard of care for these patients, and they all get it. So effectively, Sarepta wasn't doing anything incremental for immune suppression, even though they're giving very high doses. And as they dose rapidly, as they became a commercial product, I think eventually they caught up. And so what did they have to do in that case in agreement with the FDA, add sirolimus. Well, guess what, that's what we're already using. So our immune suppression is prednisone, which is a corticosteroid and sirolimus. That's what we've had from the beginning. We have not had to make a change. We talked to the DSMBs who are connected to some of these companies and said, anything you're hearing, should we be making any adjustments? And the answer was no. But you're -- I hate to put it in Goldilocks terms, but we are just right, not too much, not too little. And I would also say that it's -- we should get beyond talking about it's an AAV9 thing or it's a capsid thing because it wasn't capsid in either case. And it was immune suppression. And this speaks to the broader being vigilant about immune suppression, total dose, empty/full capsid, monitoring, how you're monitoring them in the immediate post-dose period, how you're monitoring their steroid taper. Many of us have like internalized that. We're just doing this day in, day out. And sometimes it takes a small slip up from somebody to bring this back into focus again. We feel very good where we are. And at the big picture total field level, we just have to always remind ourselves that at this point, between the 2 commercially approved AAV products that have the most patients, ELEVIDYS and Zolgensma, more than 5,000 patients have been dosed in more than 50 countries with AAV -- high-dose AAV gene therapy and the number of patients who have died and all AAV gene therapies is still less than 1%. It's a fraction of a percent. So the benefit that have been seen by patients around the world with these severe diseases versus terrible, always terrible outcomes is it's still a minuscule fraction. And so we just needed to put that into perspective.

Yes. That makes sense. I wanted to talk about a webinar also that you recently hosted discussing sort of measuring protein expression, which is obviously important for gene therapies. But maybe talk about some of the challenges in doing that and some of your sort of solutions to that problem.

Yes. So I mean, why do we do that? I mean, one is I think there's some -- protein measurement is uniquely important and it's also uniquely challenging. And so -- and there are differences between how different companies are doing it. So we thought it was the right time to do it. Why is it uniquely important? Well, first, it's our first indicator of efficacy. The very first thing we get is like protein, whether protein or RNA expression. So the biopsy data is really important. And so we take that seriously as a leading indicator of downstream efficacy. It's also uniquely important because we just talked about earlier, the FDA has said that protein can be an important surrogate marker for accelerated approval. So being able to measure that and being able to measure that consistently and accurately is super important. And so for those reasons, very important to make sure that we get this right. And then I'll also say it's somewhat challenging because most people are used to in gene therapy that the patients are homozygous, they inherited a defect from both parents. They're not producing any of their protein. And so they're starting from 0. Well, in those situations, it's actually quite -- it's quite a bit easier to both measure and to visualize even the extra protein that's being produced from the vector. But in both of our programs, and we had to learn this with the first program. In both programs, we had to figure out -- the patients -- the average patient is heterozygous, and they're producing an abundant amount of naturally occurring protein, 30%, 40%, even 50%. So how do you measure your -- the effect of your product against that backdrop? So we had to think about that, and that's why it was uniquely sort of challenging for us. So one of the things we did is we paired up with -- this is going back to now several years ago, paired up with Mike Previs, who is one of our guests on that as a world expert in measuring MYBPC3 protein. It was his papers that drew us to like, okay, this is the way to do it. We paired up with him. We successfully deployed those methods. We compared our methods like mass spec, which we believe is highly sensitive and the best way to do this with other methods like Western blot. And it was clear that you get much more interpretable and consistent information with mass spec compared -- and not just mass spec, but mass spec and normalizing to like another protein myosin that's in the cardiomyocyte versus from Western blot, normalizing to something like GAPDH. So we had that insight going into the MYBPC3, the 201 study. We deployed them. We like the data we're getting there. We'll present more of that at the AHA. And then we applied that to PKP2 as well. Those methods work very well for us. And so -- and they are now also working very well for us on the PKP2 side. Two of the other companies working in PKP2 gene therapy, Rocket and Lexeo, they're using Western blot. They are using their own methods. And that might make -- so there will be differences in the way the data is presented, and there will be -- it will make it harder for investors to compare head-to-head. It will be more like apples and oranges. Everybody will be able to say we're producing some protein, right? That's no surprise. But we will we be able to say, can we compare their data set to their data set? Could we compare their normal average or lower or upper bound to our normals, right? Maybe not because we have differences in methods, even though we're all dealing with the exact same population. So for those reasons, we wanted to put out there our methods and why we believe in our methods and other challenges that we had to solve along the way, how do you deal with a pinch with fibro-fatty replacement in it and things like that. So that was the motivation behind that.

Makes sense, and that was very helpful. Maybe we can switch to 201 HCM program. You shared some early Cohort 1 data. I think 2 updates there from the MyPEAK study. So maybe just talk about that data and what you've learned.

Yes. I mean, so we've done -- we're very happy with where we are in that program. I already mentioned the operational progress we've made. We presented initial data on that program back in December of last year, just a webinar for investors. A few short months later at the American College of Cardiology, we had a presentation by Milind Desai, who is the lead investigator on this program at the Cleveland Clinic, meaningful additional information versus December. What we were able to show at that time is that all 3 patients, we -- the first 2 out of 3 patients, sorry, that we had evaluated, we had evidence of protein increases from 8 weeks to a later time point. We had a robust RNA expression that was in line with some of our peers, including Rocket. Even at half the dose, we had robust transduction. We had -- so overall, we're happy with the biopsy data, RNA protein and transduction. We're happy with the safety data. And so that the safety profile was well tolerable. Any events we saw were consistent with other gene therapies and the effects of immune suppression. Everybody continued, no proarrhythmic effects of the gene therapy, no cardiotoxicities. So we're quite pleased with the safety profile. And then we saw on the clinical efficacy side, all 3 patients -- so 2 out of 3 patients had normalized their cardiac troponin I, which is an important blood-based biomarker of cardiac stress and injury. And so normalization is good. Then we had -- for all 3 patients, they had improvements in one or more measure of hypertrophy, like meaningful improvements. And then all 3 patients had gone from New York Heart Class II or III to New York Heart Class I. So even at this early time point, even at this first dose, we were already beginning to see signs of benefit. And so we're quite pleased with that. And then, of course, we're looking forward to presenting additional data at AHA later this year.

And that was going to be my next question. Just when you present at AHA, just what additional data should we be looking for from Cohort 1 as well as how...

Yes. So on Cohort 1, we're going to have -- by that point, all 3 patients in Cohort 1 are at or beyond the 1-year mark. So that's an important milestone. When we talk about getting full cohort data, you're not only talking about all 3 patients, but the more mature time point. So all 3 of them will be at that more mature time point. Something important that we didn't have with regards to protein in the updates to now, we didn't have the benefit of a baseline biopsy. That was just a clear learning. We needed to have the baseline biopsy. And so now when we did the update in AHA, the third patient in Cohort 1 has a baseline biopsy and a post-dose follow-up biopsy and then all patients in Cohort 2 have a baseline biopsy. So you're going to get meaningful new information on safety because we announced DSMB clearance, but now we'll be able to cover that in detail. We'll get meaningful information on protein for both dose Cohort 1 and dose Cohort 2. You're going to get more durability and deepening of the effect of -- from Cohort 1 patients. And then on the Cohort 2 side, biopsy safety, but we're not making any commitments on the clinical efficacy parameters because it's just too early for that right now. So it is a meaningful update even from December last year to March of this year to November of this year. It's a steady drumbeat of data update, but very meaningful updates each time.

And -- so for Cohort 2, you'll have the baseline plus some future point in time?

Baseline plus early biopsies as well as the safety and what effect, if anything, does dose have on the safety profile...

Can you remind us when you take the biopsies for the protein? Is it like 3 months? Or what's that...?

So we have flexibility. We had announced that last year that we have a lot of flexibility there. So we could take it as early as in the first 8 to 12 weeks. We could take it as late as 26 weeks. And that's the first time point post dose. And then there's another time point at about a year mark where we also have flexibility. It could be a little bit before 1 year, it could be a little bit after 1 year. But for the first dose cohort, this will be, by definition, baseline plus the early time point. Now interestingly, what we saw in the first dose cohort is an increase in RNA and protein over time. So whatever we show here will be the early time point. You can compare that to the later time point from the low-dose cohort and start to make some projections, and I think meaningful comparisons can be made.

And with the early sort of look at the biopsies, is that enough time to sort of see a meaningful change in the protein from baseline, do you think?

We look forward to talking to you after AHA, right? So that's -- I don't want to be the witness too far down the path of like what we're going to share there. But we just overall think it's a meaningful update.

And then since we're looking at sort of protein expression over time and you're starting somewhere different from baseline, what's -- I think it's difficult to answer, but just what's the change in protein expression over time that you think sort of will drive a benefit or what's meaningful?

Yes, it's a good question, actually, and we also covered this in the methods discussion that we're not trying to aim for some magical threshold. And I would say that through a couple of different lenses. So there's not like a number. We were asked this a lot last year. And luckily, because it has the benefit of being true, we've been consistent on our answer to this since even before we had clinical data that we don't think there's a single magical threshold that we need to achieve that. The goal of gene therapy is to give each patient more above what they have. We can approach -- we can see that from our preclinical data where at a certain dose, you get 100% wild-type protein, and you get maximum benefit. But even at less than 100% wild-type protein, you're getting significant benefit. We can see that through the data from our first few patients, right? We weren't showing 50% increase in protein. We were showing 5%, 2%, 4%, like those kind of numbers, and we were still seeing some of the benefit that I shared with you that we presented at ACC. We look at it from the perspective of our peers, both Lexeo and Rocket, modest increases in protein expression, pretty dramatic improvements in LVMI and other measures of disease. So it does -- overall, the picture seems to be that a little can go a long way in gene therapy in general, but in particularly in these cardiac programs. And the final thing I would say about protein levels and thresholds is the FDA has not asked for a threshold. So in the alignment that they have announced with both Rocket and Lexeo, they said that you can use protein as a surrogate endpoint as well as reduction of LVMI. On reduction of LVMI, they did set a threshold, greater than 10% is considered clinically benefit and outside the noise of echo. And so they said, that's your threshold. But on the protein side, there is no threshold that either of them has to achieve to convince the FDA. So I think we're just looking to continue to demonstrate that we can add protein and then show the clinical benefit, measured a couple of different ways.

Got it. So after you share this update at AHA, just sort of talk about next steps for the program. Do you keep adding more patients? What does that look like?

That's a great question. And I think we'll be in a better position to talk about that after the data release. But big picture is we're glad that we have the DSMB clearance to start to dose in parallel whenever we choose to do so, whether at the first dose cohort or the second dose cohort. We're glad that we're generating the data that we're generating. We can continue adding more patients and/or we can prepare to engage with regulatory agencies about what's that path going to look like for us? And is that path -- what does that look like for children who we've been talking about for a long time? And can we confirm accelerated approval possible with protein expression and LVMI? All of that will go into our thinking about what's the right next thing to do. Right now, I think we have an opportunity to let the dose cohort 2 data mature and to see with the benefit of dose, do we see differences in protein? Do we see differences in RNA? Do we see differences in efficacy parameters, right? If the answer is yes, that means one thing for what you choose as your pivotal dose. If the answer is no, it's within the range of noise. So how does that look relative to safety? So we have more to learn from dose cohort 2 before we make decisions about what to do in terms of dosing more patients and how many more and should we do it before or after regulatory feedback? So right now, we're giving no guidance on what we're doing in terms of dosing because we've achieved what we want to for now, and we have -- we can now learn from what we've already done.

Okay. Maybe we can move to PKP2. That's your 401 program. And then maybe you can just talk a little bit of -- give us some background on that program and maybe the disease as well.

Yes. I mean it's our second program. We're very excited about it. So TN-201, that's the leading genetic cause of hypertrophic cardiomyopathy. TN-401 is addressing the leading genetic cause of arrhythmogenic cardiomyopathy. It accounts for about 40% of all ARVC cases, and that translates to about 70,000 patients in the U.S. alone. It's a severe disease. We -- one grew some statistic for this disease is about 4/4 of patients. The first manifestation of the disease is sudden cardiac arrest and death. So you find out that you have the disease when it's too late. That's just a terrible statistic. We can do better. We also understand the genetics of the disease. It is a disease of haploinsufficiency as a result of the mutation, they're missing or have deficient levels of the protein. And so our goal with TN-201 is to simply add some of that missing protein, restore function. Now these patients will -- the hallmark of the disease is this arrhythmia. It shows up in premature ventricular contractions, nonsustained ventricular tachycardia, sustained ventricular tachycardia. They all have ICDs, eventually, they get shocks. Incredible -- that is incredible impact on their quality of life, both the exercise restriction that they're put under as well as the shocks that they experience and the fear of shocks. And so we have an opportunity to address that. There is no treatment available that addresses the underlying genetic cause of the disease. And so we're advancing TN-401 to try to do that. Most of the patients -- in this case, unlike TN-201, all the patients are adults. So they present in their 20s and 30s and 40s. And so a very different disease in many ways from TN-201 and -- but exciting opportunity to do some good...

Yes. And you're planning to share the initial sort of Phase I data from your RIDGE study in the fourth quarter of this year. So maybe talk a little bit about the design in terms of the number of patients and as well as some of the key endpoints and...

Yes, very similar design. Very similar design as the TN-201 program, 3 patients at the first dose cohort and the dose is the same, 3e13 vector genomes per kilogram. And then we already have cleared that sort of sentinel dosing in the first dose cohort. And now we are dosing at the higher dose cohort, which is exactly the same as TN-201's 6e13. So also important from a safety context that we're generally operating at lower doses compared to some of our peers who are in the 1e14 range. And so then in terms of endpoints, look, safety first. And then -- so that's also very consistent with the TN-201 program, biopsies, all patients get baseline and post-dose biopsies. So we'll be getting protein, RNA and measures of transduction. And then in terms of efficacy, that's where it starts getting different, right? Over here, blood-based biomarkers like cardiac troponin I, NT-proBNP less prominent compared to HCM, things like heart thickening, it does happen in these patients, but that's less of a prominent feature. The hallmark of the disease is the arrhythmia. And these patients have an incredible background level of premature ventricular contractions or PVCs, like more than 500 a day. Some of them have thousands a day. And that is what is a leading indicator of other things that are going to end up happening, whether it's the sustained or not sustained ventricular tachycardia and ventricular fibrillation. So PVCs are happening every day. So that also provides a great dynamic biomarker to see the impact of gene therapy in addition to potentially preventing the remodeling of the heart that's happening, adverse remodeling of the heart or prevention of fibro-fatty replacement. But that -- those are longer-term endpoints that are going to take a while to mature. But I think some of these nonsustained ventricular tachycardia, PVCs, these are things that we might be able to measure whether through a patch or through the ICDs, a lot of different ways to measure that. So those are some of the things. And of course, we'll be looking for patient-reported outcomes, New York Heart Class and other quality of life instruments.

When you share that initial look at the data, will it include all...

Well, that will include all of that. We'll clarify that. That's everything that we're studying, that design is similar to HCM. We designed the study to make sure that we are capturing all this information because there's always a chance that a program like this slips into a pivotal study and then you want to have captured all of this data and captured over many years. But the initial data release is going to be more like the data release we did last year for TN-201. First 3 patients -- all 3 patients have a biopsy with a benefit of baseline, obviously, extensive safety information. And then it's not lost on us that 2 of our peers have already presented data and both of them shared early changes in things like PVCs. So there's probably at some level -- even though we have not guided to any clinical data, but there's probably not an unreasonable expectation that we're going to share something there. And -- but that's what we're...

And then the follow-up on the patients roughly would be out to a year or less than...?

No, less than a year. So this is the -- this is, like I said, more comparable to the cohort last year when we did our initial update on 201 is that there -- all 3 patients are not at the 1-year mark. 201, the data we're presenting at AHA, all 3 patients will have at the 1-year mark. This program is one step behind. So no, not all of them will be at the 1-year mark.

And then just interpreting the protein expression, should we think about that sort of the same way as you described for 201?

Yes. I think that's like -- the goal is to give each patient more. We're going to look at it multiple ways. We look at transduction, so vector copy number. We look at RNA expression, we look at protein. We also look at other ways, immunohistochemistry, can we look at the desmosomes, can we visualize that? So yes, we have a lot that gets from the biopsy. And the goal is similar, get each patient above their own baseline and get closer to the normal range, but we're not trying to get into the normal range any more than any of the other gene therapy programs that have ever been approved have gotten their patients into the normal range of protein. That's just not our expectation. It's not the physician expectation. It's not the FDA's expectation.

Makes sense. And after you give this initial update, sort of what are the next steps you just...

Key dosing. Obviously, we're already dosing the patients at the higher dose cohort. We announced that as part of our release earlier this year. So we're on track to enroll the high-dose cohort. And then the other next steps, I would say is, I think among our peers, we're the first to be also beginning to expand ex U.S. So we are activating sites in the United Kingdom and preparing to dose patients there as well. And the other really important thing that's happening in the background is we do have the largest natural history study in the world. We've been quietly building that up over the last couple of years. So we're at a point where we have more than 190 patients enrolled in the natural history study, all of them with a PKP2 mutation. And these are all patients who are alive and being prospectively followed, plus we're collecting their retrospective data, so their past history of medications, shocks, et cetera. This is a larger natural history study than the other 2 peers combined. It is a very rich data set, gives us deeper disease insights, gives us a better way of thinking about -- we think, a better way of thinking about surrogate biomarkers for accelerated approval as well as full approval. And of course, these are patients who are at some level interested in what we're doing and could provide -- they are and have been providing patients in the RIDGE-1 study where we're dosing them and could be that source of patients for future pivotal studies, both in the U.S. and ex U.S. because we're enrolling from multiple countries. So that's what's next for the program, continue dosing patients, continue to generate safety and efficacy data and biopsy data, continue to harvest and mine the data from the regulatory -- from the -- sorry, the natural history study, continue to monitor the data from our peers because we're not operating in a vacuum. Yes, it's all execution and data.

Yes. Great. Maybe in the last just few minutes here, I can ask sort of a couple of these macro questions, asking all our companies. So there are 3, but I don't know if we'll get through all of them, but just in terms of like China rise in biotech innovation, just how are you thinking about your competitive position there? And will this influence your sort of R&D strategy in any way?

China rising is a good thing. It's a good thing for science. There's some great science happening over there. It's not relevant to us today in that we don't have any competitors to our knowledge coming from China. So it's not a -- we have -- the competitors are right here in our backyard in New York. And so we don't worry about China from a competitive perspective nor -- I actually think that's -- there's an opportunity there. There's 1 billion people. There's a lot of patients with these mutations that we care about who are probably there and hoping to also be -- the benefit from treatment. So I view that -- I think China rising is an inevitability. It's been happening by many different measures. And I don't think we should view that as a threat because our job is to advance science for patients. Anything that advances the science and anything that improves patients' lives is good. And if that just means an entire nation is kind of beginning to contribute to that and put their shoulder behind that, I view that as an absolute good thing. We're not naive that increases overall dynamics and maybe in the future competitive dynamics for us. But in the near term, I think there's more to learn from and benefit from than to fear.

Yes. Makes sense. Second question, just how are you currently leveraging artificial intelligence or thinking about AI's future disruption...?

AI. I forgot about the AI question. So look, actually, I think that's another one where it's like -- we've already been quietly doing this in the background without much fanfare. So as you know, we have a small molecule program, TN-301, that's going after HDAC6. It's a highly selective HDAC6 inhibitor. So where did that come from? Well, it turns out our conviction around the cardioprotective properties of that target came from an unbiased phenotypic screening of human iPSC-derived cardiomyocytes in the background of a genetic defect, BAG3-deficient cell line. We were screening these cell lines, characterizing their phenotype and screen like thousands of molecules against them to see which one might change the phenotype. And guess what, that was generating more images than we could possibly analyze with the human eye. So what do we use? We used imaging algorithms and AI to do that and to help characterize the improvements. And that worked extraordinarily well. And in fact, the story of that discovery process using AI is -- was the cover story of Science Translational Medicine a few years ago when they published it. So that's one way in which we're already using AI. Another way, and we have a collaboration with a very major tech company on the use of their AI algorithms for capsid engineering efforts. So we had some of our own homegrown efforts, but now we're collaborating with somebody who's got a lot more data, a lot more algorithms and a lot more computing power to say, can we screen hundreds of millions of variants and then from that, get to capsids that are better than what we've been able to do on our own? The short answer is yes. And that is -- so those are 2 drug discovery enabling efforts that have already happened or are happening right now at the company. I'm a huge believer in AI. I think it's going to -- but what we -- I can also say what we've learned from that process is you cannot -- it doesn't happen on its own. You need the people, you need the wet lab work for that to become real. So I view these as complementary and incredibly exciting for the future. What was your third one?

It was actually the FDA, which we touched...

We already touched on. There you go. We already covered that. It's all good.

And we're out of time as well. So why don't we leave it there?

So are we popping open the Corona now or later?

So thanks so much, Faraz. Appreciate your time today.

I appreciate your coverage. You did great work for us. Thank you.

Thank you.