Editas Medicine, Inc. (EDIT) Earnings Call Transcript & Summary

Good morning, everyone, for 40th Annual JPMorgan Healthcare Conference. My name is Cory Kasimov. I'm the Senior Large-cap Biotech Analyst, and it's my pleasure to introduce Editas Medicine, and Chairman and CEO, Jim Mullen. Please note that following the presentation, we will move right into a Q&A session, where you can send in your questions via the conference portal, and I'll do my best to work them into the conversation. So with that, Jim, thanks, as always, for joining us today, and let me turn things over to you for an update on Editas.

Thank you, Cory, for the introduction. And to everyone, welcome to the Editas Medicine presentation. I was appointed as CEO 11 months ago, and at that time, I had a few objectives. The first was to assess our science and the evolution of the science and gene editing, where is our technology differentiated and where should we invest in the platform; second, build the executive team and the leaders below, Mark Sherman was recruited as CSO; Bruce Eaton appointed to Lead Strategy and Business Development; Chi Li recruited to lead our regulatory strategy and operations. They, in turn, have attracted even more talent. Third was to focus on execution. This is everything from clinical trials, operations, CMC to integrate a cross-functional project teams. And lastly, chart a course for new products as well as how we will create value through partnerships, licensing and products that Editas owns and develops. Over the next few minutes, I'll describe what I found, where we are today, where we are going and how we will create value. You've all seen these safe-harbor slides before. I make -- I may make forward-looking statements within the meaning of the Federal Securities Law. Actual results might differ materially from those projected in such statements. Please refer to our securities filings for additional information concerning factors that could cause actual results to materially differ from those in the forward-looking statements. Editas Medicine has a highly-differentiated gene editing delivery technology platform. Our foundational science and capabilities are very broad. We use proprietary CRISPR enzymes, coupled with proprietary RNA chemistry, to make efficient, high-precision edits. Our technology is advanced to the point, where we can make multiplex gene edits for cellular therapy programs and multiple in vivo chain edits. We've developed a multiplex gene edited-induced pluripotent stem cell platform, with the promise of off-the-shelf cell therapies across a spectrum of diseases. Delivering the editing machinery to the right cells and organs, is a challenge for any gene editing, and we employ multiple methods, AAVs, RAPs, LNPs, in vivo, ex-vivo and cell therapies. And all of this is supported by proprietary bioinformatics analytics that allows us to design and select the best solutions for a given situation, the right edits and the right cells with the right delivery. We're able to maximize efficiency and fidelity of the desired edits, so-called, on-target edits, while minimizing or eliminating the potential for undesirable off-target edits. In 2021, we achieved, in vivo, proof-of-concept with EDIT-101. Leber congenital amaurosis is a leading cause of inherited blindness in childhood. The initial trial data demonstrated clear evidence of successful delivery and editing with meaningful improvements in vision. The quotes below from patients and investigators, increase our enthusiasm to push further and try higher doses. I'll read one from Michael Kalberer, "It has enabled me to navigate a plate of food and stab food a little bit easy. If I look down at a plate of food, and there is a spoon or utensil in it, I can see the edge of the utensil on the outside of the bowl or plate. So those changes are very significant to me." In the fourth quarter, we completed the adult high-dose cohort, and thus far, we have not seen any dose-limiting toxicities and the reported adverse events have been attributed to surgical procedure and did resolve. The numbers sometimes give in the way of illustrating the significance of the improvement. Here's what one patient experienced. On the top row on the left, is what that patient could see before treatment, on the right is what they can see now. Going from only able to see broad black and white lines to being able to see a large letter, is a significant jump, the ability to read with magnification. Below is an example of the same of patients' ability to navigate a maze at different light levels. Upon enrollment, this patient could only navigate to an exit with a bright light, typical of lighting in an office or a retail establishment. At lower light levels, such as a dim hallway, they were unable to complete the task. After treatment, they were able to navigate the complicated course with multiple turns and obstacles at the lower light level, the dim [Audio Gap]. Independent movement is an enormous quality-of-life improvement for both the patient and their family. NPR interviewed two patients last year, and I recommend you hear what they had to say in their own words, and you can find that link on our website. Our progress was also highlighted as one of the top breakthroughs last year by the American Association for the Advancement of Science. So needless to say, we're very excited by these results, and we now need to determine the right end points for a registrational trial. So these are the goals for EDIT-101 in 2022. On the left is the trial design. Just to remind you, the goals are on the right. It's first testing in pediatric patients that will get started shortly; provide a clinical update in the latter half of the year, which will include 12-month data on the mid-dose adult cohort; 6-month data on the high-dose adult cohort; and expand patient enrollment in one or more of the previous adult cohorts, and this expansion will help us design the registration of trial and select appropriate end points. Last year, we finalized the drug construct for EDIT-103 for a form of Autosomal Dominant Retinitis Pigmentosa, another disease of the retina. This is a disease leading to blindness, typically later in life, although a significant fraction of patients experience onset of symptoms in their early years. There are no approved treatments for this disease. To treat the [indiscernible] form of this disease, it's necessary to knock out the disease-causing mutant gene and then replace that gene with a functioning gene, as illustrated on this page. We accomplished this with a dual AAV approach. This unique approach, which we've tested in vivo to knockout replace the rhodopsin gene, is tested in nonhuman primates. The knockout of the rhodopsin gene and the retinal cell can only occur, if the components for the replacement gene are also delivered to that same cell. In other words, knockout and replace can only occur together. The replacement gene corrects the structural protein necessary for proper rod function. And very importantly, this addresses more than 150 mutations in this gene that cause [ rho ]-associated Autosomal Retinitis Pigmentosa. On this page, we show some very impressive data on editing in nonhuman primates. So the right two graphs showing the results of the editing. The first graph shows that we accomplished virtually 100% productive editing. The second graph shows that these edits result in production of 37% of protein levels, which is believed to be therapeutically-effective level. By the end of 2022, we expect to be well advanced in IND-enabled studies. We also have several other preclinical in vivo gene-editing programs. For Usher Syndrome 2A, we've redeveloped the initial construct for EDIT-102 and increase the editing by 350% over our initial construct. Also, this is the first time to my knowledge that anyone has used a Cas12a enzyme, packaged in an AAV, for delivery. We're also working on several other larger, undisclosed indications in the eye, taking advantage of our experience in ocular diseases and our range of delivery solutions. The graph on the right illustrates productive editing and relevant ocular cells, using several of our enzymes, which opens up larger ocular indications. There is a tremendous opportunity for gene editing ocular disease, but it doesn't stop there. We are beginning to work in other diseases, outside the eye, and we'll start to describe those later in the year. One area that I don't discuss in detail today, is manufacturing. As you know, the ability to scale up and reliably produce these complicated products at reasonable cost, is a challenge. One of the advantages of starting in diseases of the eye, the doses are small, and therefore, the cost and scale are not barriers to commercializing products. We will build upon our production experience expertise in the eye as we advance to diseases in other organs. I want to pause here for just a moment and illustrate the significance of what's happening. As we demonstrate the ability to achieve editing in target cells at therapeutically-relevant levels, the cumulative learnings provide a gateway to many more and larger unmet needs, both inside and outside the eye. The value of this initial success with EDIT-101, extends well beyond the value of that indication. Now I'll turn to our two autologous cell transplant programs with EDIT-301. We have developed a single approach to treat both sickle cell disease and beta thalassemia. Our approach mimics naturally-occurring mutations, which cause hereditary persistence of fetal hemoglobin. Patients who co-inherit one or more of these protective mutations, have no disease or have significantly less severe sickle cell disease or beta thalassemia, where they are essentially asymptomatic. Because mother nature has validated this approach, we believe this is likely to be a safe and durable approach to treating sickle cell disease and beta thalassemia. We are editing the regional [indiscernible] human [ fetal hemoglobin ] promoter in patients, who don't have one of these naturally-protected mutations, to create a change that increases fetal hemoglobin, similar to the hereditary-persistent fetal hemoglobin, which should reduce or eliminate disease in individuals with sickle cell disease or beta thalassemia. This is accomplished with our highly-efficient and specific-proprietary Cas12 enzyme. We believe the choice of editing site, plus the editing specificity and efficiency afforded by our Cas12a enzyme, could lead to a safer and more durable result. On this slide, our data to support our hypothesis. The left two graphs illustrate the very high editing efficiencies we achieved with our proprietary Cas12a enzyme and the corresponding expression of fetal hemoglobin. The right two graphs show the increase in total globin messenger RNA and the corresponding protein produced. So the current status of EDIT-301 is summarized here. For the sickle cell disease program, we have begun treatment in several patients, have successfully edited cells for the first patient and are on track for dosing in the first half of 2022. The beta-thalassemia IND was cleared by the FDA, just before Christmas, and we're in the process of setting up the clinical sites, RFD approvals, patient screening, et cetera, and expect to dose our first patient in 2022. As you can see, the trial designs are quite similar, and the initial objective is to assess [indiscernible] safety. The efficacy endpoints differ between the two indications. For sickle cell disease, we will be evaluating annual rate of [ basal-occlusive ] events and other endpoints. And for beta thalassemia, we will evaluate transfusion independence. Now I'd like to describe our rapidly-evolving capabilities with induced pluropotent stem cells or iPSCs. What's described in this page, is our EDIT-202 product. This is an engineered NK cell for the treatment of solid tumors. For this construct, we make 4 edits: 1 to improve adaptive immune response; 1 to overcome tumor microenvironment resistance; 1 to improve activation, proliferation and cytolytic activity; and 1, to improve persistence. In our process, we multiplex edit the iPSC, pick a clone, fully genotype the clone and evaluate growth, differentiation and stability characteristics of that clone. We then create a master cell bank. From there, we expand and differentiate the cells into the final product, in this case, an NK cell. In principle, we can do many more different edits, and we can also create other cell types for other diseases. This process is greatly facilitated by using our proprietary SLEEK technology, which is described on the right-hand side of this page, but I won't discuss for the sake of time. Here, we demonstrate the effectiveness of the edits. The top graph illustrates the persistence of NK cells over time without exogenous cytokine support, focus on the orange line. The bottom graph shows the antitumor activity, the engineered NK cells, when administered with trastuzumab, and the orange line shows the reduction in tumor burden with EDIT-202. On the righter image mice, which showed tumor clearance out through 31 days. The far right panel, outlined at orange, shows the EDIT-202 plus trastuzumab-treated mice. We are working on additional constructs, including constructs with [ CARs ], and we believe this is a mini platform, where NK cells can be engineered for many different solid tumor types. Once the first program is reduced to practice, or in other words, GMP clone is created, the process for differentiation and expansion is scaled up and robust, follow-on programs should be faster and easier. Multiplex editing of iPSC expertise was one of the jewels I found, when I became CEO. And I quickly realized the broader significance of this platform, well beyond NK cells. As our expertise grows, we're eager to begin work in other cell types and other diseases. As many of you know, we have an ongoing partnership with -- since 2015, with Bristol-Myers Squibb in alpha-beta T cells. BMS has opted into 6 programs, one development candidate is in IND-enabling studies. They're leveraging many of our technologies, our proprietary Cas9, Cas12a, [indiscernible] design, et cetera, to create autologous and allogeneic approaches in [ immuno-oncology ]. To date, we received over $125 million in payments, plus potential for milestones and royalties in the future. Our pipeline of products is expanding quickly. Earlier, I discussed our four occular programs, and we have many more ocular opportunities. These products are wholly owned and have the potential to create a very nice business. We're now in a position to explore in vivo indications, outside of the eye, and we're beginning that work now. Our ex-vivo sickle cell disease and transfusion-dependent thalassemia programs are in the clinic, and we expect to have initial clinical data in sickle cell disease, later this year. And lastly, we are rapidly building expertise in product candidates and the engineered cell therapies, starting with our BMS collaboration in T cells and our NK programs derived from edited iPSCs. 2022 will be an exciting and pivotal year for Editas Medicine. In the EDIT-101 program, we expect to dose pediatric patients, we will expand one or more previously-completed cohorts, design the registrational study and select end points. We will have 12-month data in the mid-dose adult cohort and 6-month data in the high-dose adult cohort. Our Retinitis Pigmentosa program should be well through IND-enabling studies. We expect to declare the final construct for USH2A product, and we intend to advance another ocular program. We will have initial clinical data in sickle cell disease program, the first beta-thalassemia patients will be dosed, and we will begin IND-enabling studies in EDIT-202, our first of a series of iNK programs. And at the same time, we'll continue to support BMS in their T cell immuno-oncology programs, as they advance the first program towards the clinic. And we will continue to develop new and [ innovative ] technologies and techniques for gene editing and delivery. All of these products and technologies are underpinned by a broad intellectual property portfolio. We are the exclusive licensee of foundational CRISPR Cas9 and Cas12a patents. These enzymes are used in many of the clinical stage gene-editing programs of some of our competitors, including those employing base and prime editing. Our intellectual property spans essentially all diseases, where CAS9 or Cas12a are used, and our products are supported by over 220 issued patents and 800 applications covering composition of matter use and process. And this coverage includes all important markets, globally. Now you may ask, how relatively small company with this many products and this much technology, will remain focused and create and capture value. I've been in this business for four decades and have lived and extracted the lessons of company and value build. We will own some areas. Right now, the ocular programs look very promising. We will partner and collaborate to extend our reach, access capabilities, accelerate programs and as a source of funding. We'll license our technology patents in areas that are promising but low priority for us or outside of our reach. We'll bring in technology and products that complement our programs. And we'll maintain focus, optionality, agility to pursue the most promising products, as data evolves. The investment highlights of Editas are these, we have highly-differentiated proprietary gene-editing delivery technologies, which we continue to extend. Our editing technology can address the vast majority of genetic disease. We have studied and looked at this question very carefully, in the latter part of the year. 2021, we demonstrated the ability to effectively edit in vivo. This unlocks additional ocular editing opportunities as well as opportunities in other organs. 2022, we expect to show initial clinical data for sickle cell disease program. We will develop and present additional data, demonstrating the power of our iPSC-derived off-the-shelf engineered cells platform and move the first product towards the clinic. We'll continue to work closely with BMS to advance their T cell programs in immuno-oncology. So a very busy year, indeed, ahead of us. I've been CEO for 11 months. It's clear to me that what attracted me to this company at the beginning, to become a Board member, continues to be true. Gene editing is one of those once-in-a-generation technologies that will spawn many important products. The science and technology at Editas, are exceptional. We have a rapidly-advancing expanding pipeline. We're building a team of scientists, physicians and executives that know how to build a company and capture and create value. Thank you all for your attention. I hope to talk to many of you as investors in our future. And now, I'll turn it back to Cory, and we'll go to Q&A. Thanks.

Perfect. Thank you, Jim. Let me remind everyone that you have the ability to ask questions as well in the portal, and we have some in there already. Welcome to the rest of the team here as well. And I guess, I'll start right off with the portal. It's a bigger-picture question, who kind of speaks to Jim, your comments about, sort of, the future of gene editing. And the question is, given the innovation in the gene editing space, how do you think about Editas' strategic positioning? And what are the key strengths of the company's platforms?

Yes, Cory, it's a great question, and it's a question that certainly came up a number of times, over the course of the last year, as I've been CEO. And we spent a lot of time studying this precise question. Particularly, I think, people are talking about base editing, prime editing, and where does our technology fit. And we did a very detailed review of, sort of, all of the, sort of, genetic diseases, if you will. And how accessible those are with the technologies that we have or what we believe are relatively straightforward extensions of technology we have in house and concluded that, really, the vast majority of the opportunities can be addressed with what we have. That's not to say that there are a few instances, where base or prime editing will, sort of, have a unique application, but we think those are relatively isolated. And there are some places, where we'll overlap what we can do. But I'll just point out, sort of, two things that would be hard to do with base or prime editing. One is the rhodopsin program, where we're really knocking down and replacing a gene and, sort of, taking care of 150 mutations in one [indiscernible]. And then the other one I'd point to, is sort of the sickle cell disease, where we're actually addressing or mimicking a number of naturally-occurring mutations. And the base or the prime will, sort of, go after those, one by one. So we feel pretty good. In fact, we'll continue to work on extending our platform technologies there. But more to the point, I think, we view that the bigger challenge is now going to be delivery. Our editing capabilities are very good. It's just can you get the editing machine, where you want it to go. Mark, perhaps you want to add some comments?

No, exactly, that, I think, we are very confident in our ability to very carefully and specifically design [ guys ] that result in high on-target editing. And we're working -- continually working on additional delivery mechanisms to reach other targets base and other indications that we currently don't work on.

Much of that delivery innovation takes place in-house versus, sort of, across the industry that could benefit all?

I think, some is taking place within Editas, for specific purposes. But as you might imagine, there's been an explosion of innovation and creativity in the LNP space, for example, which we are tapping into.

Okay. A few more questions keep popping in the portal here. One's a follow-up on this big picture one, but it gets a little bit more specific. What are the pros and cons between Editas and specifically Beam's approach towards sickle cell and CAR T? The underlying designs are very similar.

Do you want to take that, Mark?

Yes. I'll take the sickle program. So we're targeting a region of the promoter that is known to be mutated, either point mutation or deletion, in the [indiscernible] persistence of hemoglobin patients. And so by mimicking that, we feel that we can get a robust elevation of HbF. It's done in a very safe way, meaning, the specificity of the AsCas12a, essentially at least, only on target editing, given the desired outcome that we want.

And then, you know the -- keep up with this portal. EDIT-202 does knock out [ HLA 12 ] with some of the other iNK competitors do. How does this allogeneic cell product evade host immune system?

So that's a good question. I think the -- as you saw today, EDIT-202 is a base configuration, which, we feel, will have utility in itself, across a broad range of solid tumor indications. We can expand upon that, meaning using SLEEK technology, plus other general CRISPR knockout technology, introduce other things like [ AlloShields ], CARs, chemokine-homing receptors and things like that. And so we feel that, that will be a follow-on product configuration that can be customizable for specific solid tumor indications.

Okay. And then to ask on EDIT-101, I wanted to first talk about the anticipated BRILLIANCE update in the second half of this year. So we'll obviously get an update on the 3 adult cohorts across low-, mid- and high-dose levels, as they're all enrolled. Any expectation for preliminary data on the pediatric mid-dose? Or is it going to be cutting it [ a little pros ]?

So I think the honest answer is that we've had absolutely no concerns regarding enrollment in the patient population. Following RD 2021, we had an awful lot of parent and patient outreach, looking for possibly enrolling patients in the trial. One of the challenges, however, is that a lot of the interest is coming from parents, who have children, who are just beginning to lose their vision in the first couple of years of life or before school age. Now that we've had successful data as well as safety, successful data from the [ big-dose ] cohort and demonstrated safety in the high-dose cohort, one of the things that I have at the moment, is the luxury of being able to focus much more on efficacy. And so as a consequence, we're being very selective in the enrollment of children as to those who can provide us with reproducible and consistent, repeated measurements over time. With that in mind, the pediatric patient population is lagging a little bit. So the end of the next year may be a little bit early to provide a [ fourth ] data readout.

Okay. When you do have those pediatric patients in there, can you speak to any unique challenges that might be specific to this group, such as the ability to compete -- complete efficacy assessments?

Well, that's exactly the point, is at the moment, we've got a pretty laborious list of efficacy assessments that need to be done by the patients, even the adults are finding it a long and tiring day. We really want to have kids that are just old enough to be able to follow instructions, clearly, to be able to do the measurements on a reproducible fashion and don't start getting overly tired and not able to participate. So as a -- that's really probably the biggest challenge at the moment.

Okay. And then, Jim, in your talk, you discussed the need to determine the right endpoints for a registration trial. Do you expect this to be pretty straightforward, based on the precedent that's been set here? Or are you thinking about some potentially alternative pathways or measurements?

I'm going to toss that one to Lisa because she explains that far better than I do.

So Cory, what was the question again? I'm sorry.

Just following up on Jim's comments during the talk about needing to determine the right end points for a registration trial with EDIT-101. Is it -- do you expect us to be pretty straightforward, given the price [indiscernible] out there? Or are you thinking through all potential alternative pathways?

We're learning an awful lot from the study, and this is one of the interesting findings. The patient -- what we're hearing back from the investigators and from the subjects in the clinical trial, is that we actually have had some significant and meaningful impact upon their daily lives. This includes things just as simple as being able to walk through a doorway and know whether the doorway is open or closed. It also includes whether or not they can walk around outside. They may be perfectly comfortable moving, [ hovering ] around in high light. But then they get lost, when it starts to get dim outside. How this actually translates to the classic measurements such as BCVA, ECVA is actually kind of a dirty measurement. The classic, can you improve your reading vision from one line to another?, is it really relevant in a patient population that can't even read the chart? So we're looking at a deep dive into the evaluation of how we can actually translate what's being reported to us to the patients, related to the outcomes that we're measuring. And that's really where we're focusing our efforts, at the moment. With both the data we've had from the mid-dose, the data we expect to have from the high-dose population, but also looking at our natural history data that we've had, just been able to identify what are the most reproducible measures.

Okay. A couple more portal questions, get back in some bigger picture topics. How are you addressing off-targeting effects in allogeneic products for regulatory concerns?

Well, with the iPSC platform, once we've edited the sales, we select a single-cell clone for further development, that clone gets extensively characterized, so that [indiscernible] moving that forward. We know that we have the -- only the edits that we want and no off-target editing. So that's pretty much takes care of itself in that regard.

Okay. And then another one, how do you anticipate your iNK program to fit within the competitive NK landscape?

I think, if you look across the landscape, we're the only company that has that combination of edits, if you look at the main competitors in the field, whether it's for liquid or solid tumor programs, they may have 1 or 2 of those edits, and then typically introduce a CAR or other ligands. So right now, with that base configuration, we feel we have an advantage. And as I mentioned earlier, we can easily add on to that with other knock-ins and knockouts for specific purposes. So right now, we feel that we've entered into the middle of the fray, in terms of these products. And we have a lot of encouragement in the properties that we're seeing from the EDIT-202 cell.

Okay. And then on EDIT-301, this is something, I know, we've discussed before, but I have some questions out of this as well. So can you speak to how you may -- how you believe you may be able to differentiate 301 in a very competitive space? Basically, where do you see room for improvement, upon the profiles of other genetic therapies that are in later stages of clinical development?

I'm just going to jump in. So what's -- the bar is high for the initial clinical outcomes, right? But people have just, for the most part, measuring vaso-occlusive events because they happen relatively frequently, and they're fairly easily measured. But that's really not the be-all and end-all of treating disease. So I think you need to collect longer-term data on durability. Obviously, on safety, to make sure that safety holds up over a longer period of time. But also starting to look at things like end-organ damage, frequency of strokes, early mortality. Other things that are really the objective of the exercise because there are patients that have severe events associated with the disease, but don't necessarily have a lot of vaso-occlusive events, for example.

Okay. And then how much data do you ideally want to collect before publicly releasing? I know, in your slides, you said that you expect an update by the end of this year. But can you speak a little bit more to that, what you'd like to have in hand?

What we'd like to have in hand or what we will have it hand? [indiscernible] Sorry, that was two different things [indiscernible].

Yes. [indiscernible] follow-up.

Yes. What we will have in hand -- obviously, you'll have some safety view on the initial patients. We should have engraftment information on the first patients, and you should start to see, sort of, the reports of the fetal hemoglobin levels. You won't have enough follow-up to have anything meaningful on things like the vaso-occlusive events. Did I get that about right, Lisa?

I don't have much to add.

I guess that means you get it right. On LCA10, can you characterize the addressable market opportunity here?

Yes. LCA10 is sort of mid-single digit thousands of patients in the U.S. So it's a rare disease. It's not a huge indication. When you go to rhodopsin for Retinitis Pigmentosa, that's a somewhat larger population.

Okay. And are you taking steps to identify patients? Or has that happen purely naturally out there, in terms of the diagnosis with a particular genetic disorder?

These should -- patients, which basically means children present, usually fairly early in life, sometimes in the first year or two, where parents observe that there's something not right because they've got stigmas or difficulty tracking any [ gaits ], et cetera. So they do get diagnosed relatively early in life. I don't know how many of -- what percentage of those get actually genotyped at that stage. Probably, that will increase, and that's something we would look at because we will need that information. That's part of our inclusion criteria. Lisa, you might want to add.

So we're actually working with Foundation [indiscernible] on this as well, as a number of other advocacy organizations, partly to be able to increase awareness related to the use of these genetic therapies. But we do know at the moment that at least genetic testing with the United States, is still relatively limited. So we've actually been looking into being able to provide testing upfront. One to, of course, identify patients for the study, but also to be able to bring better attention to the frequency of events or at least the frequency of diagnosis. But I do think, this is part of a big shift in techniques now because as we begin to come out with more genetic treatments, there's a much higher interest in families to actually finding out what the underlying genetic mutations are. So it is in progress.

Okay. And then, Jim, I know you didn't have much of an opportunity to discuss your SLEEK knock-in technology for the iNK program during your prepared comments. Can you talk about the opportunity -- and it's a very cool technology. Can you talk about the opportunities that this might ultimately unlock?

Mark, that is -- you love to answer this question. I'm going to give it to you.

So the EDIT-202 product that we disclosed this week, is using SLEEK to knock in at the [ GAPDH ] locus, that bicistronic [ C16 ], IL-15. We have identified a number of other SLEEK sites. So what that means is that you can use a best configuration and add into that. So it gives us the opportunity to knock in things like CARs, knock in things like cytokine receptor. So there's a lot of flexibility here to really customize the technology, and we're getting more and more experience using SLEEK, in addition to iPSCs, we can edit T cells, B cells and NK cells. And as I say, we're developing know-how and knowledge that can be applied across the iNK program. The iPSC program, more broadly. As you can imagine, iPSC cells can be differentiated into a number of different lineages. To my knowledge, there's been very little effort to date in the regenerative medicine field to edit those iPSC cells ahead of differentiating them to other [indiscernible]. So we feel that, that's a great opportunity for us.

Okay. Terrific. Well, guys, we are about out of time here. So thank you very much for participating here again, and I appreciate it and best of luck this year.

Thanks, Cory. We really appreciate it.

Thanks, Cory.

Bye-bye.