Precision BioSciences, Inc. (DTIL) Earnings Call Transcript & Summary

Thanks, everyone, for joining us. I'm really pleased to be joined by the team of Precision BioSciences, Michael Amoroso, President and CEO; Alex Kelly, CFO; and Jeff Smith, CRO. Thank you so much, guys.

Thank you for having us, Andrea. Good see you.

Michael, maybe I'll start with you here. As you think about the last 12 months, Precision has gone through a strategic transition and one that has now put you squarely on path to be an in vivo gene editing company and that's where your priority is. Maybe speak to us about what drove that decision. What has that meant to Precision as a company?

Yes, absolutely. So I think, first and foremost, Precision has always been a gene editing company. The platform that Jeff created, ARCUS is our own IP, maybe not as well-known as some of the others, but that's some of the strength that not everybody can touch and handle it. Our first programs for ARCUS that were in the clinic to your point, Andrea, were ex vivo applications, outside of the body for CAR T. And those were important programs for patients. We've had some really nice data there before we divested those programs off to partners. I think what we saw, Andrea, is the landscape changed, the cost of capital changed. And we knew that we did not -- the core capability of Precision is ARCUS. We think it's a highly differentiated gene editing platform. Really all the gene editing platforms are CRISPR-based, need guide RNAs, whether it's a base or a prime kind of derivatives. And those are good technologies. Most of them are really at the liver and doing gene knockouts. ARCUS was actually -- it can do those knockouts, but it was created to do different types of that, as we call them sophisticated, and it's like adding DNA, for example, or excisions in some of our programs of large base payers. Our early programs on eliminations. For example, at HBV getting rid of the entire viral genome. Jeff will talk to you a little bit about the technology. But this technology is highly differentiated. And what that means, Andrea, is we can apply it in much larger areas for millions of patients with afflicted diseases. So I think when the landscape changed when we got to the inflection point, we thought we would probably take our CAR T programs, just backing up for a moment, across the line with the first BLA and then partner. When we got to the inflection points around the Phase Ib time frame, we got the pivotal feedback from the FDA. We felt it was the right time at that place to partner it off. We did that with Imugene for our cancer rights for azer-cel. We did it with TG Therapeutics, who is also already in the multiple sclerosis space, for autoimmune. We thought those were really viable partners to carry it onward. But operationally, we wanted to focus fully on our in vivo capability. And that's really what Precision was built on. So -- that's where we are now, one platform. HBV is our lead program and mitochondrial disease, primary mitochondrial myopathy as our second. So it was an important pivot. I think the landscape helped us get there faster. But I think it was always the plan for Precision. And we've got a lot of feedback there, "Okay, now we understand exactly what you guys are, a gene editing company, not a cell therapy company."

Jeff, maybe I can turn it over to you before we dig into the programs here. But as Michael alluded to, the ARCUS platform, help us understand how that is differentiated from other gene editing technologies?

Sure, happy to. So really, there are 3 key advantages to ARCUS over all the other gene editing platforms. The first is the very unique cut that ARCUS generates. ARCUS is derived from a completely different scaffold protein than all the other gene editors and what we've done is we've maintained the evolved function of that base protein to be able to insert DNA using homology-directed repair. And a lot of that tracks back to the unique cut that the enzyme generates, which is a staggered cut and allows us, in the presence of repair template, to insert with really high efficiency even in nondividing cells and which allows us to tackle different patient populations than a lot of our competitors would be able to do. The second advantage is size. ARCUS is the smallest gene editor on the market. It is substantially even smaller than these nano-CRISPRs that come out. And that gives us a few advantages. Firstly, it allows us in terms of delivery, being able to deliver both by LNP and AAV to allow us to -- as Michael said, to be able to do the editing and deliver, but also to be able to do sophisticated edits beyond the liver, in other tissues. It also gives us the safety in terms of that we are able to actually be able to package a more potent, cleaner drug product in LNP like for a HBV product. And it also allows us because the protein is so small, to gain access to target sites such as in the viral DNA for the HBV program. The third advantage is what we call simplicity and the fact that ARCUS is the only single component gene editor. What I mean by that is, so if you -- if you had to deliver something to get a job done and you could deliver it all in one truck, one delivery vehicle. That's a lot easier than having to deliver 5 different parts in 5 different vehicles and get them all there at the same time. That's essentially the difference in that ARCUS is able to be delivered in a very compact way in a single delivery vehicle, which improves our efficiency and helps us lower the dose. And also, ARCUS is unique in that the DNA binding so the GPS to find the correct target site is actually fully integrated into the cutting. And so only when you find the correct site, does it activate to actually cut the target site.

Andrea, Jeff just helped me realize is my wife must be using old technologies because I have multiple packages coming to the house all the time. So thank you for that, Jeff.

Maybe one follow-up there. As the landscape has changed. There's been the next wave of editing technologies that have come about, whether it's base editing, prime editing, epigenetic editing, how do all of these approaches coexist? And there are a number of these companies that are using these different types of technologies but going after the same indications. How do you think about the interplay of all of these?

Sure. That's a great question. And I guess, first of all, I do think that there's -- there are specialized applications for each. But the way I like to think about it is in a tiered way, in terms of applicability and the scope that they can be applied. And so if you think about it like a base editor really can only go after a single base change. And -- so you're depending on the patient population that has a mutation that is a single base change. And unfortunately, for base editors, there's only 1 of 2 base changes out of the whole array. It can't even do the whole array. So I would say it is probably the most limited in scope. And then prime coming in after that in terms of being able to switch out small sections of DNA. It's able to do all of the base changes unlike base editors. It's also able to do small insertions and deletions, but in many cases, patients have mutations spread throughout a gene. And so if you want to be able to have one drug product that addresses a large percentage of the population, you need to be able to address a larger portion of the gene. So there, prime is also sort of limited. Then you get into your -- you mentioned epigenetic editors. In their case, they can turn off genes, but they can't really turn -- or correct a gene. And so if you have a loss of function that you just don't have a functional gene, epigenetic can't actually help you with that. Now in the case of ARCUS because we drive a high rate of repair -- in a process called homology-directed repair, you can actually dictate the exact type of repair that you want with the repair template you provide. And because of that, we can essentially address all of the requirements for all the other editors as far as base changes, small edits, large edits, we can replace an entire gene, we can insert an entire gene. And so in terms of that tier of scope of applicability of ARCUS is having an advantage and being able to really address the widest scope. In addition to that, as we were just saying about size, because ARCUS is so small in many cases, it's 6 -- 3 to 6x smaller than all the other gene editors. And because of that, we can actually go to not just ex vivo and liver but beyond liver to all other tissues, whereas in many cases, some of them are so large that they're sort of pigeon-holed in either ex vivo applications or applications purely to the liver.

Yes, Andrea, it was a great question. I think -- as I think about it, more simply than Jeff, I view the gene editing companies as really smart. I think they're going where they're good for the most part. I think for the most part, you don't see a lot of replication of editors. There's some, to your point, but they're really trying to say, "What does my technology do well?" And that's why I don't think there's a one winner takes all. We love the fact that ARCUS, we believe, has a wide application, one of the unique things you'll hear me talk about today, in diseases like HBV. Primary mitochondrial myopathy, 15,000 to 25,000 patients in the U.S. alone; m3243, that's the mitochondrial 3243 mutation. Our first program that we just took back from our Lilly partner, Duchenne muscular dystrophy, you're talking about large epidemiologies, part of that is getting regulators comfortable with your technology on safety. You remember we had the iECURE partnerships. So we've got the longest-standing nonhuman primate data that really helps us. But the applicability of the type of data you make is something that I think is where the different editors are trying to apply their technologies. The only other thing I would add there is you could have the best editor in the world, and we think the way we're going to apply ARCUS, we do, but you have to have the greatest delivery in the world, right? Most folks or large technologies going to liver and LNP today, and that's where a lot of the competition is. But when you go to tissues around the body, muscle, brain, you're going to need to have the right partnerships. You can't create everything yourself, the right partnerships, the capsid delivery, viral delivery. Right now, everyone is trying to figure out how to deliver for an insertion, add function, a DNA repair template nonvirally. No one's quite there yet. So I think you'll start to see differences in maybe the approach of delivery versus editor versus editor, maybe a lesser dose, if you will.

Maybe one last follow-up there since you referenced the FDA getting comfortable around the safety profile. And what are you seeing, and maybe describe to us the extent of the work that you've done to characterize off-target editing because that is so important here.

Yes, I'll start, and I'll let -- Jeff, chime in, if you will, on the off-target. Maybe you could explain ARCUS, but I'll go a little bit [indiscernible]. It's a robust process and it should be. We're going into genomes, and we're making permanent alterations. I mean that with ARCUS, CRISPRs base, prime. Epigenetic editing, silencing, that's different. I look at that a little bit more like siRNA. But when you're making a permanent edit, we have to be held to task, what is that going to mean long term for these patients. You heard the early guidance was only go to patients in dire need. Like our first program through our partner iECURE-OTC, babies with this toxic ammonia level, unfortunately, hitting early mortality. What you're seeing with the comfort level increase, and we'll talk about exactly what that looks like in a moment, is the ability for Precision. After our follow-on, our partner iECURE just [ starting in ] the disease where there's 3 million people in the U.S. with HBV. The things they want to see for comfort, on and off-targeting, how specific is your editor, is your assay development plan comfortable for them to make sure that you know, what all your on-targets are doing, but if there's any off-targets. The ability to look at the entire genome is not equal across the different editors. One of the unique things about ARCUS is it makes that unique cut where Jeff started, which gives you that overhang. And that overhang really is not created by anything else in nature. We're able to really get regulators comfortable. It's an iterative process. It takes us a while to get to a clinical candidate, but we think it matters for safety. The regulators are very, very big on the next topic of reproductive or germline editing. Will you pass this edit on, and what you're seeing there is biodistribution studies. They want to see that in genomes that are more similar to a human being, so a nonhuman primate, let's say, as well as often, they'll ask for progeny studies. Even if you don't go to the ovary and testis, you saw the early on, do the progeny study anyway. In theory, if you don't go to the ovary or the testis or the sperm or the egg, you can't have edits in your offspring. But the early guidance was, do the progeny study anyway. So we interfaced early and often with the FDA. You can't skip these steps. And I think the last part that's big is toxicology. And the toxicology has a lot to do with, again, a body size and/or genome that's similar to a human, if you can, primates. More often than not, I know there are some companies that have gone not with primates, but we think that's a good proxy for toxicity. And that's more than the editing. The editing is the on and off-target. The editing is that the reproductive of the germline. The toxicology is really what doses of these LNPs or AAVs can we deliver. And you got to be careful because one company's LNP at the same dose, one mg per kg, let's call it, is not necessarily equivalent to another company's. LNPs are different creations, but they're also how they package their mRNA and there really matters. We spend a lot of time optimizing the mRNA because we know that could add to undue toxicity. So I would say the IND or CTA process in the more nascent gene editing days, if I compare it to a small molecule, it's probably 2x, small molecule was probably 18 months to the clinic. This has been about 3 years. Now the good news is once you have that toxicology, the biodistribution of a certain type of delivery vehicle, LNP X or Y, AAV Z or M, you can now use a lot of those things and build. It's a platform scaling. So -- but every time you have a new nuclease, you're always going to need a unique off-target panel. That's their areas of key interest. Jeff, do you want to just talk quickly about on and off targeting of some of the really unique reasons we feel really good about the safety and on versus off-targeting?

Sure, so starting from the science side, as Michael mentioned that unique cut, it gives us up to a 15x higher sensitivity for determining off-target sites. And I think a key difference for ARCUS is that if we find and identify an off-target site, we can reengineer ARCUS to be able to eliminate those off-target sites. And that's where that iterative process is really built for safety and being able to identify sites and then eliminate them. And what we've gone to, Michael mentioned it, in terms of the regulators, we've gotten great feedback. They have looked at our package for safety and called it robust. They've been very agreeable with our plan. We have a multipronged way of trying to identify sites and then validating them and then identifying and seeing if anything happens as a cause of a site. Fortunately, for both of our lead programs we have not identified any off-target sites at a saturating dose. So the safety package has been very well received.

And maybe we can jump to your lead program here. And I was curious just maybe on your comment about the reproductive studies that are necessary. As you sit now in front of a CTA or IND filing, have you conducted those studies?

Yes. So the germline editing, I would say, on the competitive landscape, I'm not giving everything away, but the answer is yes, you have to do the work. It starts with biodistribution, doesn't go to those tissues. And then the question will be, do you need to do progeny work? And I think depending on the biodistribution, it's really a decision tree, right? So on that standpoint, yes, we've been very robust in our -- looking to reproductive offspring and germline. So yes.

Well, maybe walk us through, I guess, maybe for HBV, we can start there. Where that program stands, the timelines, being able to get to the clinic, maybe even the approach that you're taking, which is pretty unique.

Sure, sure, yes. So again, not to be coy, but the landscape is we do a lot of big lifting with the regulators, we want to move the field forward. But started off with all of our -- the INTERACT meeting for HBV, our first program, hepatitis B, large, large epidemiology around the world, was, do you have the right plan for proving on and off-target. This is the LNP-delivered, it's an ARCUS nuclease, to the liver. What's unique about this program, just as a reminder. Everyone says you can't cure HBV, and thus far, you haven't been able to. The standard of care is combinatorial therapy that disrupts a viral cycle downstream. We're the first approach that is going after looking to eradicate, eliminate the cccDNA, which I call the factory that makes the bad guys, that makes replicating virus. We are looking to cut that out in its entirety, okay? So the first question was on and off-target, and we had our INTERACT meeting with the FDA as well as ex U.S. agencies to say, "This is the plan for our on and off-target." We've shown last November, our lead clinical candidate at AASLD. And then we just gave an update at EASL, I believe, and Jeff can tell you about that, of our clinical candidate and the safety profile because we know there's been a lot of questions about LNP delivery. And we wanted to show, "Hey, we haven't seen the transaminase concerns with our candidate." One LNP is not all LNPs. Second, reproductive germline editing. There's definitely been an ask from the FDA on that. I'll tell you, we definitely did biodistribution studies in primates. And then the question becomes, do you need to do the progeny? We haven't divulged that yet. So I don't -- again, I don't mean to be coy, but I think we feel very complete and aligned with the FDA on that. Last, toxicology studies in primates. And that is where we're at right now. We are in toxicology. This is the last phase for us to have these results, knock on wood that they come out well. We feel pretty good because in our proof-of-concept studies, you might remember, Andrea, where we showed cutting out 99% of the virus. We did that in primates. That represented the doses. So now we're repeating it with the final LNP candidate for our clinical -- final clinical candidate at those representative doses. So we feel pretty good that we had a good proxy going into our toxicology. So we're in tox. We should finish that into Q3 here this year. And at the same time, we are in parallel contracting sites. It will be a global study. We haven't announced all the sites, but we've told the world -- we've looked at some of the early gene editing markets like the New Zealand, in the U.K., France, Moldova and we've even looked at the U.S. We got early feedback from the FDA that we could go in the U.S. Now the challenge is that the right investigator to do Phase I studies in each of those markets. So we're onboarding sites as we speak. We're going through our contracting as far as you can go before you have the approved IND or CTA. And the goal here, the [indiscernible] but -- so that we're on track to file this year, CTA and/or IND. And the stretch goal for the team is can we get first patient dose this year. That's where we're at. So we're in the final toxicology studies. We're putting together the CTA and the INDs. We're onboarding sites, and we're getting ready to treat first patient.

Jeff, maybe I'll let you comment here on the approach for this HBV program. What have you seen from the preclinical data that makes you so excited?

Sure. So first of all, as Michael was saying that I think we are -- our mode of action is fundamentally different in so many cases, all of the competitors are looking at other parts of the life cycle without really tackling the root cause of the disease, which is the underlying factory, Michael always like to say, the virus that sets up shop and generate -- keeps on continuing the infection. In our case, we are actually tackling and causing elimination and that preclinical data that has us so excited is that through simply 2 doses, even taking that down to the lowest dose that we treated, we have seen greater than 90% in the higher doses, 99% engagement of a virus surrogate. And being able to eliminate that. We also have this overlapping mesh of different animal experiments, showing every different possible aspect of HBV infection. And being able to show that we see all of the markers, s-antigen, core antigen, all those type of things decrease. But what's really encouraging is even in the transgenic models where the HBV is integrated, we see no rebound that -- after we remove all therapies, those remain low. And whereas your standard nukes after you take them off, they rebound.

Yes. Andrea, really important. We'll start in what's called the control -- patients who are on nucleoside analogs, it is the standard of care in the clinic, who are controlled. And what that means is they'll have a certain level of HBV DNA. And the goal here is a finite number of therapy and to stop all therapy. Cure, cure is the goal. Functional cure, we say once you stop therapy for 6 months, but the goal here is sterilizing cure, that they never have to come back to therapy. So we'll start on patients who are on nucleoside analogs that will keep the replicating virus at bay while we treat with 1, 2 and we can go up to 3 doses of LNP-delivered ARCUS. And then we will track, right away, you'll have safety data, within a month, on your LNP, you'll have s-antigen data. And then as the s-antigen comes down, you want to get it to a nondetectable level for 2 consecutive readings and you could stop your nucleoside analog. That is about a 2-week washout. Andrea, if we see the HBV DNA is still gone then we know we hit the factory. We know we got the cccDNA eradicated. So we're really excited. This approach has never been tried. So until you dream it, it can't happen, people say you can't cure a replicating virus. But this is the first time we're going at root cause. And when I say we, I mean, industry, industry has not gone at the root cause yet.

Maybe to that point, what would be the amount of follow-up or the durability that you would look to understand that you truly are providing a functional cure here?

So this is interesting because for the infectious disease community, functional cure means, you stop your nucleoside analogs, and you don't have disease at 6 months. And the reality is we don't have that. You've got 1%, 2%, 3% of patients. You don't have that with other therapies. And if they have it, it's not because of therapy, their immune system did something. In the masses, we don't have that in the industry. For us, due to the modality, if you understand the modality, we'll deliver an ARCUS, about a month later, you'll have your second ARCUS. And that's how we did the primate studies, 2 deliveries. Our protocol for Phase I allows us to go to LNP, remember, so no antibodies, so we can go up to 3, but we got 99% of the virus cut out with 2 doses in the nonhuman primate model. So the goal will be this: Phase I, you're looking at safety right away. You'll know that within a month, you're looking at s-antigen right away. Is the s-antigen coming down? You see it coming down, you're excited, then you got to say, why is it coming down? Because s-antigen comes from the cccDNA. We call it 2 heads of the dragon, but it also comes from integrated disease and hepatocytes, okay? So you could be addressing 1 of those 2 and decreasing s-antigen. Once we get the s-antigen -- and we'll do biopsies later in the study, but the fast way to get that answer, s-antigens down, you get to undetectable. As long as you have a second reading of undetectable 4-weeks apart, you can stop your nucleoside analog. Here's the golden question. No one's been able to look at this yet. If there's about a 2-week washout with nukes that we know, disease comes back. Jeff was talking about the transgenic model. We stopped the nukes after the ARCUS treatment, and it didn't come back. So you will know from a serum marker, HBV DNA. If you stop your nukes on day 1, 2-weeks later, you have washout. By week 3, you can measure. Week 4, if the HBV-DNA has not come back, your s-antigen stays suppressed. You know you got it, the mechanism. Now the industry wants in the infectious disease, the field, show me that durability at 6 months. That really comes from the therapies that frankly have been nonideal, downstream viral disruptors. So we will absolutely track and look for 6 months. But Andrea, if I get to a point where they're off nucleoside analogs and the HBV DNA didn't come back in a month, then you should feel good about the durability for 2, 3, 4 and 5, up to 6 months because the idea is you've gotten rid of the factory. So -- but 6 months is something that will not go away. We will definitely be tracking that, okay?

Great. Maybe we can turn to -- I'm going to skip over PMM today.

Okay, I understand. I get it.

In the interest of time, let's talk about DMD and where that program stands now that you've taken back that from -- the conclusion of the Lilly-Prevail.

Sure. So just to make sure the group understands, our second program is PMM, and it will be editing the mitochondria, huge unique advantage for ARCUS there, nothing with a guide RNA can cross the mitochondria. So this is going to muscle. So very important. This is myopathies where patients don't have ATP, they don't have energy. Think of the DMD, type of walking tests, things of that nature. So that's an important function. That's our second program. So we've learned a ton about muscle delivery and some of those unique applications of ARCUS. Andrea, to your point, we did take back our programs. We had a great relationship with Lilly. We're appreciative. Not all marriages last forever. We did a lot of great science together. Lilly has got a ton of program to choose from. And we opted to take back the lead program Duchenne muscular dystrophy. That, of course, is an ARCUS delivered to muscle. What we're doing there is we're cutting out exon 45 to 55, a 500,000 base -- defective base pair, and we're basically restoring native dystrophin gene. The approach is out there today, and I mean this kindly, thank God for companies like Sarepta and others, but they're really suboptimal. You have an approval for micro-dystrophin approaches with a failed primary endpoint. That patient unmet need is huge. We take that seriously, so speed to program is important. We took the program back. We haven't divulged too much. We took the program back from Lilly. It was later stage preclinical. So it's at that stage where it's probably ready for those last steps like toxicology, which we talked about, the last steps in our HBV program. Right now, we are assessing whether we go it alone or whether we do this with the right partner. And you say, "Well, Michael, you just took it back from a partnership. Doesn't that mean you want to do it alone?" Potentially, we're very committed to our first 2 programs. That gives us a cash runway with those first 2 programs all the way through Phase I to the second half of '26. We can look at the alternative funding mechanisms or I think the way we would think of partnership at this time, if we look at partnerships, twofold, do you increase our capability for any program. This is beyond DMD. So maybe the novel delivery mechanisms. I think we feel for the DMD program, we have the delivery mechanism. Do you increase our fiscal capability, our time to clinic. So when we look at partners, that's what we're thinking about. We're assessing things like maybe instead of out-licensing, a co-development partnership, so we can get to markets around the world as we set up clinical because, of course, we can't do all clinical programs. This would add a third on our own. These are the things we're still assessing. We're super excited about. This is still the first gene editing approach as we see it where it's at in its preclinical timeline. We have a suboptimal therapeutic landscape, unfortunately, for these patients. These patients are still highly afflicted, terrible disease, they're dying. And we do think a gene editing approach that restores normal dystrophin or as close to normal dystrophin as you can get to, keeping the protein domain is super important. Exactly where we're at operational, I don't have an update for you yet. It is a highly competitive landscape. So we're going to be smart about when we come out and talk about our approach. But we are -- very frankly, we're still assessing some unique partners, and we're still assessing the capability of go it alone.

Maybe for people who haven't yet seen your data, just walk us through really quickly what you have seen, what makes you so excited that this could be more optimal than therapies that are out there?

Yes. So Jeff, no one better than you to do it. I mean obviously, we're short on time, but can you talk about what would be unique of this approach versus microdystrophins? Exactly what we're doing with the DMD program.

So the easiest way to think about it is for that protein, it is essentially your shock absorber for your on [indiscernible] front end and you need the back-end functional, and the middle part is basically this [indiscernible] in the front end and in the back end, but minimal [indiscernible]. What we're doing is by cutting out a section of this gene, and it's one of the largest genes in the human genome, we're restoring function, but we're restoring function with a nearly fully functional, fully length protein. And because of that, we expect greater stability, greater function. And what we have seen from that in the mouse disease model is an 86% restoration of function upon treatment. And so that's what has us very excited is that even from our -- some of our pathology, the treated mice, the muscle actually looks better and it gives us lots of reason to believe that the DMD program is definitely working and we will [ see ] good tremendous results.

If I can just add maybe to Jeff's point. One of the things you want with Duchenne muscular dystrophy treatment is durability. And so far, we've also shown the ability to edit the satellite cells, which means that the future progeny of those satellite cells will also have the same edit. And that to us is a really great sign about the durability of our approach for DMD.

Yes. I think this is an example of restoring function and the size advantage Jeff talked about with ARCUS as well as some of the cut advantage that allows that after that -- you're sending 2 ARCUS in 1 AAV, and you're allowing a perfect religation to bring back that normal protein domain. I'm sorry, go ahead.

No, I was just going to ask if you could put into context the 86% relative to others?

Well, tough to do versus other gene editors because there's no other gene editor in this space. But Jeff, can you speak a little bit to dystrophin approaches? And it's not apples-to-apples, I want to be fair. But the dystrophin approaches, any thought of kind of percentage of expression they're getting?

Well, I almost think expression is probably the wrong aspect. This is 86% of normal function compared to a wild-type mouse. So -- which at least from the vendor that ran the experiments, the best I can give you is that they also run for a lot of our competitors, and they did share that our data was exceptional in terms of that restoration of function.

Maybe in the last couple -- about 10 seconds we have here, [indiscernible] things you'd like to leave us with, things you want to make sure that people are focused on over the next 12 months?

Yes. First, thank you. Thanks for having us. Second, key inflection points. Look, remember, Precision was thought of as a cell therapy company by many, and that's why maybe our valuation is still a little bit [indiscernible] that's okay, with the engine it could. Proprietary rights are the only ones that can use ARCUS. Applicable for more therapeutic areas. We're the only gene editing company today that I'm aware of that has 3 shots on goal for clinical data, clinical data, proof in the next 24 months. That's first in OTC through our partner [indiscernible] further in the clinic as we speak. That data could be this year or the beginning of next. And our first organic program for HBV, clinical data in the first half of the year and the second half, the follow-up of it. And then third, the primary mitochondrial myopathy program, data in the first half of '26. So we sit here with a 2-year window, where we've got 3 shots on goal. I don't know any gene editing company right now that's got 3 shots on goal in big epidemiologies which are uniquely all multibillion-dollar markets.

Perfect. Well, with that, thank you all for joining us.

Thank you.

Thank you, Andrea.