Good morning, everyone. My name is Gil Blum, and I'm a Senior Biotech Analyst here at Needham & Company. Welcome for joining our second day of the Needham Healthcare Conference. It is a pleasure to have with me today Precision BioSciences team, Alex Kelly, the Chief Financial Officer, and Cassie Gorsuch, the Chief Science Officer. With that, Alex, feel free to start your presentation. Great. Thanks very much. Good to be here, Gil, and thank you to the Needham team for inviting us to present at the conference. Cassie, if you can advance to the next slide quickly. Just as Gil introduced, I'm the CFO at Precision, and Cassie Gorsuch is our Chief Scientific Officer. Next slide. Before I begin, I would just remind you that some of the statements that Cassie and I make this morning might be considered forward-looking statements. As a result, you should refer to our 10-K, which was filed in March, for any forward-looking statements that you should be aware of. With that, next slide. What is Precision BioSciences? Precision BioSciences was founded as a spinoff from Duke in 2006, so we're celebrating our 20th birthday this year. Our co-founders, Jeff Smith and others, developed the ARCUS gene editing platform, and that has been the source of our company, and we are dedicated to improving the lives of patients through our in vivo gene editing platform. As I mentioned, this is proprietary to Precision BioSciences. Our co-founder, Jeff Smith, is also our Chief Research Officer, and our team has now 20 years of experience of using this ARCUS gene editing tool and using protein engineering to create the ability to edit in a variety of different tissues and for a variety of different diseases. As you can see, we have a large intellectual property estate with this ARCUS platform, with more than 75 patents issued to date for ARCUS. Unlike other gene editing tools, ARCUS is derived from a homing endonuclease I-CreI, which is found in green algae. We believe that has several advantages, but it's also derived from green algae to drive efficiency gene editing. Next slide, please. Okay. Our in vivo platform right now, we're focused on two programs that are in vivo gene editing. The first one is for Hepatitis B, PBGENE-HBV. We are engaged right now about a year into our ELIMINATE-B trial, which is a phase 1/2 trial studying patients with chronic hepatitis B. This is an important disease area and one that we're very excited about. We presented data last November, and we expect to present additional data in 2026. The second program is also wholly owned. That is for PBGENE-DMD for Duchenne Muscular Dystrophy, a very important disease area with a high unmet need. Even though there are existing treatments that are coming to the market in the last few years, there is still a very significant need for patients for a treatment that provides a long-lasting and functional benefit. Now, through our history, we've also had a number of partnerships that are relevant. The first is with iECURE. That is in vivo gene editing also. It's using ARCUS gene editing to treat a disease called OTC deficiency, and OTC deficiency, when it occurs in neonates in its severe form, can be very life-limiting. Unfortunately, three-quarters of the children who have severe OTC deficiency when they're born, they don't make it past their first birthday. Having a treatment for these children is critically important. iECURE, our partner, announced last year that they had achieved a complete clinical response in the first patient treated with ECUR-506, and that is the drug that uses ARCUS gene editing. This is a gene insertion program, so it's, from a technical standpoint, much more challenging than what other gene-editing tools can deliver. I've also listed here two other programs which date back to our CAR T programs, which we previously had in development at Precision BioSciences, but we have outsourced them or outlicensed them to Imugene in the case of oncology and TG Therapeutics in the case of autoimmune disease. Both of those companies continue to make very good progress with those programs, and as a result, we have generated milestone payments to Precision BioSciences for those programs, and that's helping us fund the ELIMINATE-B trial as well as the FUNCTION-DMD trial. Next slide. Okay, just real quick, talking about the need in these two populations with hepatitis B and Duchenne Muscular Dystrophy. Both of them are multibillion-dollar product opportunities because they're addressing large unmet needs. In the case of hepatitis B, there are more than 300 million people around the world with chronic hepatitis B infections, and in the U.S. alone, there are about 2.5 million patients who have chronic hepatitis B. Market opportunity is very large there, and the need is high because the standard of care currently does not deliver a high degree of functional cures in many patients. In fact, a single-digit percentage of patients can get to what's called a functional cure in this disease. That's our first drug. The next drug is, as I mentioned, PBGENE-DMD. The prevalence here in the U.S., we're looking at 300,000-400,000 patients globally, and about 15,000 is the prevalence in the U.S. Each year, about 550 boys are born with Duchenne Muscular Dystrophy in the U.S. Very important need. Our product, PBGENE-DMD, addresses up to 60% of the patients who have Duchenne Muscular Dystrophy. Next slide, please. With that, why don't I hand it over to Cassie, and she can walk you through these two programs in a lot more detail. Cassie? Thanks, Alex. I want to touch first on really the platform that Precision was built on, our ARCUS gene editing technology. As Alex mentioned, we have a proprietary gene editing technology at Precision that our scientific founders, including Jeff Smith, developed. There are a couple really important differentiators that make this a really attractive gene editor for therapeutic applications. I've highlighted those differentiators here. The first is the cut. Really what we mean is the way in which ARCUS nucleases cut the DNA. It's a four base pair, three-prime overhang, which allows us to take advantage of homology-directed repair, which is really inaccessible with other types of gene editors in non-dividing cells. We think it's really this particular feature of ARCUS nucleases that have led to the success that Alex described in the OTC deficiency program through our partners at iECURE. The next differentiator is the size. ARCUS nucleases are very small, about 1,000 bases of coding sequence, and the small size matters when we think about gene editing from a delivery perspective. Having a small protein allows you to deliver both by LNPs to the liver, like we do for our hepatitis B program, but as well as through AAV delivery for ex-liver tissues, like we are in our Duchenne program. ARCUS nucleases are actually so small we can put two ARCUS nucleases in a single vector, like we are in our DMD program, and I'll show you that in a moment. The last differentiator is the simplicity, what we call simplicity. What we mean by that is that ARCUS is a single component gene editor, so it's one protein that we engineer to recognize a DNA target site and cut that site. One protein that needs to be delivered. There's no guide RNA involved. It's the protein itself that actually interacts with the DNA and cuts the DNA. This really streamlines efficiency and gives us a lot more flexibility in the types of technical edits that we can take on. It's really through these differentiated features that we think make ARCUS a really excellent therapeutic gene editor. Let's take a couple minutes to talk about our first wholly owned in vivo gene editing program for chronic hepatitis B. There's been significant investment in the hepatitis B space over the last couple of decades from a clinical development perspective. Really, I think when you look at what have we learned as a field, I think it's summarized in this slide. Where the field has really been focused from a therapeutics perspective is targeting components of the viral life cycle downstream of the root source of the infection. When hepatitis B virus infects hepatocytes in the liver, it establishes a viral DNA reservoir in the liver called cccDNA. This cccDNA is what gives rise to new infectious particles, and cccDNA persists forever in chronically infected patients. However, we've never actually been able to therapeutically target cccDNA itself. Instead, the vast majority of clinical development has been focused in these purple circles, in these downstream components, whether it's blocking RNA from becoming DNA, like nucleoside analogues do, or ASOs and siRNAs focused on S antigen reduction. We've been focused on downstream components of the viral life cycle, never actually focused on targeting the root source of the infection. What we've learned is that even when you combine a number of these different antivirals or immune modulators targeting these downstream components, functional cure is rarely ever achieved. Today, standard of care, as Alex mentioned, nucleoside analogues achieve functional cure 1%-3%, which means patients are left taking medication their entire life and remain at risk for serious liver complications like cancer or cirrhosis. We've designed PBGENE-HBV to actually go at the root source of hepatitis B for the first time ever. PBGENE-HBV is a lipid nanoparticle that contains an mRNA encoding an ARCUS nuclease. That ARCUS nuclease has been designed to cut and eliminate cccDNA and cut and inactivate integrated HBV DNA. By targeting the viral source with our ARCUS platform, we can then shut down production of downstream antigens, including the production of new infectious virions. By eliminating and targeting cccDNA directly, now we can look at shutting down, at the viral source, the viral infection. PBGENE-HBV is actually uniquely positioned within the therapeutic landscape to achieve a complete cure by actually eliminating the viral source, thereby preventing the potential for viral relapse downstream and hopefully addressing those long-term liver complications I mentioned earlier, like cirrhosis and hepatocellular carcinoma. We're testing PBGENE-HBV in a Phase 1 study called ELIMINATE-B, and the study design is illustrated here on the slide. There's a Part 1 and Part 2 of this study. Part 1 is really dose finding. What we're looking for in Part 1 is the optimal dosing regimen that allows us to stop NUCs and demonstrate functional cure or cure in these patients, the ability to maintain viral suppression off all treatment. What we've conducted so far and presented data on for this program in November at the liver meeting was data from our first three cohorts: Cohorts 1, 2, and 3. As you can see here, these cohorts were designed to test ascending dose levels of PBGENE-HBV. Each participant in this study is enrolled, that is HBeAg-negative patient who are on standard of care treatment, so controlled with nucleoside analogues during their treatment course with PBGENE-HBV. Each patient receives three dose administrations of PBGENE-HBV spaced eight weeks apart and at ascending dose levels from Cohort 1 to Cohort 3 of 0.2. We also started enrolling Cohorts 4 and 5, which look at a shorter interval of four weeks. We have the potential to look at administrations beyond 3 as well. Really the goal of this Part 1 of this study is to identify that optimal dosing regimen that allows us to achieve viral suppression after we've taken patients off therapy. With that optimal dosing regimen in hand, then we can move into Part 2 dose expansion, where we'll test that dosing regimen in a larger number of patients. Importantly, in Part 2, we will also be collecting paired liver biopsies from each participant in this study. In Part 1, we are collecting optional biopsies from patients, and I'm excited to share a little bit of that information today. In Part 2, we'll really build out our biopsy data set. The goal of this study, as I mentioned, is really to demonstrate the ability to provide a finite course of treatment with PBGENE-HBV that results in a sustained viral suppression off all therapy. Looking first at some of the data coming out of this study, here we're looking at the tolerability profile for PBGENE-HBV. What we found through these first three dosing cohorts is that PBGENE-HBV has been well-tolerated with repeat dosing. I should mention that as of the data cut, we've enrolled patients in all three cohorts. We completed dosing all three administrations in all three patients in Cohorts 1 and 2. The data are interim data from Cohort 3, where we have all three patients receiving their first administration, and one patient also had received their second administration as of the data cut. Across all of these 22 doses administered, we've seen no dose-limiting toxicities. The types of adverse events that we have observed are consistent with LNP IV infused products, primarily infusion-related reactions that occurred on the day of dosing and resolve quickly, within about 12 hours after dosing. These include things like chills, fever, headache. We have also observed transient transaminase elevations. You can see here a Grade 2, Grade 3 ALT, AST respectively. Those occurred on the same dose in the same participant, and resolved within about a week after that administration. They occurred very proximal to the infusion and were not associated with any clinical symptoms or bilirubin changes. The last thing to note on the slide is we have observed a couple cases of hypotension as we've increased the dose. These have been manageable with reactive saline. Because it was reactive in this case, it was considered a Grade 3 adverse event. Since observing these types of events, we have implemented infusion parameters like prophylactic saline that have really helped control some of the hypotension events we've seen. Overall, the adverse event profile has been as we would expect with an LNP-type drug. They've been predictable, manageable, and overall good tolerability. Now shifting to efficacy. I'm going to summarize here the efficacy data. As we've increased dose level between Cohort 1 and Cohort 3, we did see dose-dependent durable S antigen declines. In Cohort 1, we saw activity in all three patients, which was very exciting. Even at our lowest dose level, all three participants showed substantial S antigen declines during their course of treatment, indicating PBGENE-HBV is active even at our lowest dose level. One of the three participants in this cohort has actually sustained about a 50% S antigen decline. The other two patients returned near baseline levels. This really told us that for the first time in this one of three patients, that gene editing could lead to durable S antigen declines in a permanent mechanism as you'd expect with gene editing. What we concluded from these other two patients was that we didn't achieve enough viral reduction of that reservoir in the liver to sustain the reduction. We look to improve upon that by increasing the dose level. In Cohort 2, again, we saw activity in all three patients. Now we also see durability of the response in all three patients, with all three patients showing substantial S antigen decline from baseline. Cohort 3, as I mentioned, is interim data, but all three patients in this cohort were also achieving a indication of activity by substantial S antigen declines. At the data cut, all patients had achieved durable S antigen declines, and we're continuing to follow these patients through the rest of their course of treatment. I mentioned that we are also collecting optional biopsies in part one of this study. We were really excited to have a participant in Cohort 2, our 0.4 mg/kg dose cohort, who agreed to a baseline and post-treatment biopsy. In the biopsy, we were able to demonstrate for the first time ever, proof of gene editing against a viral DNA target. When we looked at the DNA sequence, the viral DNA sequence in this participant after two dose administrations, we could see the formation of PBGENE-HBV-mediated mutations in the DNA sequence or indels. This demonstrates that the S antigen declines that we were observing in circulation were the result of the direct mechanism of PBGENE-HBV mutating viral DNA in the liver. This patient did go on to receive their third administration and saw a further S antigen decline, suggesting the ability to accumulate viral DNA gene editing clinically, just like we observed pre-clinically. So this is a really exciting proof of principle, proof of mechanism for PBG ENE- HBV utilizing biopsy data and correlating that to serum biomarkers like S antigen. So where we are today with this study is that we are continuing in part one of this phase one study through dose optimization. I mentioned earlier we've opened Cohorts 4 and 5 and started dosing patients in these cohorts. These cohorts are designed to look at the lever of time between administrations and the effect of that lever, and so shortening from an eight-week interval to now a four-week interval, we'll continue to evaluate both the safety and efficacy in these additional cohorts. And again, the goal really is in part one to define that optimal dosing regimen to achieve viral suppression and then move quickly into part two dose expansion. Now I'd like to take a couple minutes to introduce our PBGENE-DMD program. As many people are familiar, Duchenne Muscular Dystrophy is a really devastating progressive neuromuscular disorder. Kids who are born with DMD typically are normal developing for a couple of years, where they learn to walk, they learn to run. I've heard from parents this referred to as sort of the golden years with a kid with DMD, where there's really not obvious signs of the underlying disease. However, around four, five, six years of age, these kids start to demonstrate muscle weakness that becomes progressively worse with time. Ultimately, these kids lose the ability to walk and are wheelchair-bound, and ultimately, all of them will die from this disease, either from cardiac failure or respiratory failure. The unfortunate truth is we really haven't changed the prognosis, this disease course. Despite clinical development, we really haven't been able to achieve meaningful clinical benefit for these patients. The unmet need persists. When you look at the tissue level, what causes DMD is the loss of a protein called dystrophin, and dystrophin is an essential protein in muscle. It allows for healthy muscle to recover from damage. It serves as a shock absorber within muscles. You can see on the left an image of what a healthy muscle would look like where dystrophin is present, and on the right, when dystrophin is absent, you start to get muscle wasting, deposition of fibrosis and fat versus myofibers. This is what's really leading to the loss of muscle function in these kids. It really is because of genetic mutations in the dystrophin gene that result in the loss of dystrophin protein that lead to DMD. At Precision, when we sought out to develop PBGENE-DMD, we looked at the therapeutic landscape and wanted to improve upon the existing therapies, and our goal was really, as indicated here. This was the north star for us. We wanted the product, PBGENE-DMD, to be applicable to most patients with DMD. This is a challenge for therapies like exon skippers that are very limited in the number of patients that can actually be addressed. We wanted to be able to improve muscle function over time. The way to change the long-term prognosis of this disease is to be able to provide a long-term, durable muscle function improvement, and that has not been achieved therapeutically either with exon skippers or with micro-dystrophins today. We're excited about some of the preclinical data that we have in mice demonstrating the ability to provide long-term, durable benefit as well as actually seeing increased muscle function over time. The reason that we think we're able to provide this differentiated long-term durable benefit is because the protein that's produced as a result of PBGENE-DMD gene editing is a near-full-length dystrophin protein. This near-full-length dystrophin protein is a much fuller protein than what you see with the micro-dystrophins, which are severely truncated forms, and the protein made by PBGENE-DMD has known function in humans because it occurs in a subset of Becker Muscular Dystrophy patients who have overall good prognoses. We know that the protein works in humans, which was a big unknown with the micro-dystrophins. Finally, thinking about from a patient perspective, access and ability to receive this type of drug, we wanted it to be a single administration therapy to really reduce the burden on patients of going through a therapy like this. This is really what we sought to achieve with PBGENE-DMD, and in our view, achieving this type of product profile would really demonstrate a significant advantage over the existing therapies in the DMD space. I mentioned just a moment ago that the protein that's made by PBGENE-DMD is a near full-length dystrophin protein, and that's really illustrated here on the slide. The top is the full-length dystrophin, healthy dystrophin that is made as a result of a healthy dystrophin gene. Under that is the dystrophin protein that's made by PBGENE-DMD gene editing. You can see it retains 80% of the full-length dystrophin, and achieves all of these different functional domains. These different color-coded boxes illustrate different functional components of the protein, different binding domains of the protein. The protein made by PBGENE-DMD retains all of these different functional domains. The micro-dystrophins, a couple of them are shown here. What you can see is that they're severely truncated, about 30%-34% of the full-length dystrophin. Even going back to some of the initial papers that first described these micro-dystrophins, we've known for a long time that these shortened, truncated versions do not function as well as a fuller length dystrophin protein. They are compromised in their functional capabilities. Based on natural history studies, we expect that as little as about 5% of the functional dystrophin protein, the near full-length dystrophin protein made by PBGENE-DMD, could provide therapeutic benefit in DMD patients. On the low end, that's really our therapeutic target, would be about 5% dystrophin protein expression. We know that this protein that's made by PBGENE-DMD is functional in humans because it occurs in a subset of humans within the population. These humans are Becker Muscular Dystrophy patients who have the exact same genotype that will be made as a result of PBGENE-DMD editing. What you're looking at on this slide is the clinical presentation of Duchenne patients on the left that we just talked through, and these Becker patients with this exact same mutation and the exact same protein that's made by PBGENE-DMD. These Becker patients can live into their 60s or 70s. Many of them are mildly symptomatic or even asymptomatic and ambulatory their entire life. They demonstrate normal respiratory function with some myocardial involvement but often manageable with medications. As you can see, this clinical presentation is a significant improvement over the clinical presentation of a Duchenne patient. We think this is really proof of principle that the protein that's made by PBGENE-DMD can be meaningfully functional in humans because of this clinical presentation in these Becker patients. We've generated a whole host of preclinical data to support this DMD program. I'm going to talk through a couple of components that we think are really exciting as we head into the clinical stages of this program. What you're looking at here is mouse data from our preclinical package. We utilized a DMD diseased mouse and treated these mice with PBGENE-DMD, a single administration, followed them out to nine months. We collected a cohort of mice at three months as well as nine months and evaluated how much dystrophin protein could be visualized after treatment with PBGENE-DMD. Here you can see across heart, calf, and quad, a significant improvement in the amount of dystrophin protein. Here we see up to about 25% in the skeletal muscle of dystrophin protein after treatment with PBGENE-DMD. What's really exciting is consistently across these tissues, we see an increase between three months and nine months in the amount of dystrophin protein. We think this is likely due to two reasons. One, the fact that this is a near full-length dystrophin protein. We know that it's a very stable protein and can accumulate over time. We've demonstrated preclinically that we can target satellite cells, which are the stem cells in skeletal muscle that give rise to new myocytes and new myofibers. We are very excited about this increase in dystrophin protein expression across all of these different tissues, and significantly above that 5% threshold, more in the 20%-25% dystrophin protein expression here. We've also correlated that dystrophin protein expression with significant improvements in force output or functional capability in these muscles. What you're looking at here is a force measurement readout or functional assessment in these mice. The light gray bars on the left demonstrate that these DMD mice have a deficit in the ability to exert force compared to healthy animals, which are the bars just to the right in the dark gray. Those are healthy individual mice, demonstrating that the disease model does have a functional deficit. When you treat with PBGENE-DMD, you can see at these two different dose levels, the ability to increase force output from three to six months and maintain that force output out to nine months, long-term durable benefit. The ability to achieve near healthy levels of force output, significant improvement over the DMD diseased untreated mice, really nice correlation of both the biomarker of dystrophin and the functional outcome here now in the force measurement. I'm excited to share that we recently received IND clearance for this program from U.S. FDA, and so we are currently underway of activating sites and getting our clinical study up and running with the goal of dosing our first patient on this study in this quarter, before the middle of the year. The way the study is designed, it's a phase 1/2 study, and the primary endpoints are really around safety. Characterizing the safety and tolerability of PBGENE-DMD. We will also be looking at dystrophin protein expression through biopsies collected at baseline and at 12 weeks and 52 weeks post-treatment. Using these muscle biopsies, we'll be able to look at the expression of dystrophin protein after treatment with PBGENE-DMD. The goal is really then to demonstrate biologic proof of concept, biologic activity through the dystrophin biomarker, and then correlate that with exploratory endpoints, including a number of different functional outcomes. We are enrolling kids aged two to seven, and so we have age-appropriate functional and developmental assessments incorporated into our exploratory endpoints with the goal of correlating that biomarker with functional benefit. This is the overall trial schema. As is typical with AAV-based therapies, there will be a staggering between dosing of the initial patients on this study. Between patients one and two, and two and three, we expect about an eight-week interval in terms of the staggering between dosing. We're enrolling boys who have mutations in exons encaptured between exons 45 and 55. That's the region that PBGENE-DMD actually targets, and so it would be applicable to patients with mutations in this region. We will be utilizing a comprehensive immunosuppression regimen to really promote the safety and tolerability of PBGENE-DMD dosing. Once we've got the initial data collected from these first three patients, we will be able to then, looking at that data, utilizing that data, move into the Part 2 expansion cohort, where there will be fewer restrictions around dosing interval between patients. Really our goal, as I mentioned, is first patient dosed in first half of this year, with the ability then to share initial safety and biomarker data on multiple patients by the end of 2026. We're working with really world-class clinical sites across the U.S., and we really prioritized utilizing these very well-known sites, these DMD sites that have experience with both treating Duchenne Muscular Dystrophy patients as well as with AAV gene therapy to really ensure the highest probability of success for the study, both with physicians who have experience in both of those two key areas. It's really been a pleasure getting to know a number of these physicians and getting to work with them, and we're looking forward to partnering with them as we move this FUNCTION-DMD study into the clinical phase. Ability improvement in muscle as really the north star for us and our goal. We're excited to continue to push this program forward and really achieve that milestone of first patient dosed. Now I'll hand it over to Alex for some concluding remarks. Great. Why don't you just go forward to the next slide, and I'll hand it over to Gil. Just real quick, we've got a lot of exciting things going on at Precision BioSciences, starting with our PBGENE-HBV program. We call it the ELIMINATE-B clinical trial, and also with the FUNCTION-DMD trial that Cassie just talked about for PBGENE-DMD. We're going to have data events for these programs throughout 2026. In the case of HBV and the DMD program, as Cassie walked you through, we'll expect that first data set coming by the end of 2026. We've got a good cash runway right now. We had $137 million at the end of the year, and we expect that that cash runway will carry us through 2028. We'll see all these data points that we're talking about here in 2026, but also we'll have data events in 2027 and beyond. With that, let me hand it over to Gil. Thank you, Alex. Thanks for the presentation and maybe a couple of quick questions. First of all, on the HBV program, just for us to better understand, do you need to completely eliminate all viral DNA in order to basically get rid of the underlying disease? Even if a little bit is left, would it build up over time? Yeah, I think that's a fair question we get a lot, and I think that's the billion-dollar question. The answer is, actually, we've never had a therapy that can even ask or answer the question. This is the first time because we're going at viral source. I think to me, our goal is to eliminate as much viral DNA as possible. I would love to say we're going to achieve all viral DNA elimination. I think in the absence of achieving complete viral elimination, there is actually some clinical data that supports the potential to achieve cure without clearing 100% of the cccDNA. That data I would point to would be the Stop NUC studies, where we took HBV e-antigen negative patients who are on long-term NUC therapy, like our patients, and the intervention was really just stopping their therapy and then monitoring them. What we found was in patients who have relatively low S antigen levels, those patients, about 30%-40% of the time, went on to achieve cure. We know those patients still have cccDNA because NUCs don't clear cccDNA. What that tells us is there is a level of viral infection that can be low enough where if you take them off therapy, you can achieve a cure. I think what one potential for PBGENE-HBV would be to reduce the viral load in the liver to sufficient levels that allows for the individual to maintain viral suppression through immune control of their infection. I think there's clinical data to support that is feasible, particularly in the e- antigen negative NUC-treated patients. Question on the DMD space, which we do cover. The challenge has primarily been delivery. It's a little hard to define whether there's a huge difference between different transcripts. I buy the argument that longer is better, but that's very hard to prove out. Long way to ask, what AAV are you guys using? You mentioned immune suppression, but how feasible is this? You're already going at one to the 14th. Can you dose escalate? Is that even possible? Yeah. I didn't mention it when we went through our clinical study, but our plan is not dose escalation. When we selected the 1 × 10¹⁴ vg/kg dose level, we selected it based on preclinical data with the goal of providing both a safe dose and what we think can be maximally efficacious in patients. We're not planning to dose escalate on this study. We're using AAV9. We selected that capsid because we demonstrated the ability for that capsid to achieve satellite cell editing, which we didn't observe with all of the capsids that we tested. I think when you think about a gene editing approach, I agree delivery has been part of the problem. I will also say, I think we've seen decent micro-dystrophin protein expression that has not correlated with functional benefit, and I would point to the construct designs in that case of where we're seeing differences. I do think the truncated micro-dystrophin we've known through publications for a long time is not nearly as functional. I do think delivery is part of the challenge. I think we've demonstrated preclinically the ability to achieve both substantial dystrophin protein expression, and I didn't have a chance to talk through it, but also up to 85% dystrophin positive expressing cells within the tissues. We're seeing good distribution at the cellular level within tissues and at the tissue level across the organism. I think, really, the differentiated approach of gene editing versus a gene therapy, obviously we need to generate the clinical data, but I think there's a lot of reason to believe that the approach will be differentiated in a number of different ways beyond just delivery. Right. That is very interesting. We're at time. Thank you again for attending today. Thank you very much, Gil. Thank you very much.