In many ways, I think that Biogen needs no introduction. It's a long, well-known company in our industry. Maybe you could take a few moments to speak to the journey that you've been on to create a new Biogen and how your approach to R&D is evolving. Yes, we've been very excited to create the new Biogen. I'm really pleased because I think we are well on our way. I'll start with the fact that, you know, from a commercial perspective, the Alzheimer's launch, we are seeing some inflection points in the LEQEMBI launch. This is important because we just got approval for subcutaneous maintenance, which we think is a very important option for patients. We've also begun our rolling submission for the subcutaneous initiation. That means patients, hopefully, once we have the outcome next year for subcutaneous initiation, and we already have it for maintenance, patients could actually have an autoinjector that they take at home. I think it provides optionality because they can still choose to come to an infusion center. We know there are many different segments of patients as well as health care providers. The other important catalyst in the field that we've seen is that blood-based biomarkers have, you know, as you know, FDA approved the first one, the IVDR, but there are many available today. I think what it does for the field is it provides the option of being tested. That has many downstream positive consequences because it can free up neurology chairs. It can free up the reason to have a CSF or a PET. Actually, we've seen data that the number of blood-based biomarker tests has gone up exponentially. There has been an increase in the positive outcomes from CSF and PET. We think those could be related. It's important. The other piece from a commercial perspective, as you know, we've launched several drugs in the last few years, all first in class. It's really been a pioneering effort. What we're really pleased about is we're seeing year-on-year revenue growth from our growth products more than offset the decline from our MS product. This is important because I think the growth products are where we are really focused. It really is looking encouraging at the moment. The R&D piece that you asked is very dear to my heart, of course. It's very important because we embarked upon a journey to curate, evaluate the total pipeline, starting from research and going into development. What we have today is a late-stage, high scientific conviction set of programs that we expect registrational data as early as next year. It's been a very important move because we've gone from low value, low probability of success to high value, high probability of success. The reason that we have been able to make that change is we are advancing programs into phase 3 and late stage based on a de-risking proof-of-concept data set. That is important. We're treating internal assets and external innovation the same. You've seen us advance litifilimab. You've seen us advance dapirolizumab pegol, both for lupus into phase 3. Very exciting, you know, potential build of a lupus franchise here. Equally, we broadened and acquired HiBio. With that, we have already initiated three phase 3 trials for felsardimab in the rare nephrology space. We are evaluating it for several other indications, including a phase 2 PMN indication that we think we can start next year. It's a very exciting time. We also did more business development with Stoke Therapeutics. You saw us have an alliance with Stoke on Zorobinursin, which we think could be really meaningful and disease-modifying for patients and children with Dravet syndrome. Here we have seen very exciting data, specifically on the Vineland Adaptive Scale. We have already started our phase 3 trial with Stoke and those patients. We also are building our pre-proof-of-concept pipeline. I'd like to focus on that next because here we have some very important readouts coming up next year. We have BIIB080, we have BIIB122, we have BIIB091, as well as we have just announced that we've transitioned an internal asset, which is an IRAK4 degrader. This is coming from our collaboration with C4 Therapeutics. Again, a great example of collaboration, but starting early. This is very important. IRAK4 is a very important node in the inflammatory pathway. We think it could be very meaningful once we get data from our first-in-human. We're looking to dose our first patient actually in a few weeks now. We think we could get important insights that could bring us into considering several autoimmune conditions, including lupus. Really what we have is we are building depth and breadth across our key franchises like Alzheimer's, lupus. With immunology, we're really going broad. We are looking at many aspects in research where we could enhance tissue delivery, but also look at different immunological pathways that could have applications in different system organ classes. Exciting times and looking forward to the next wave of potentially registration readouts next year. Excellent. Maybe we can start digging in on LEQEMBI, and congrats on the recent subcutaneous maintenance approval. Maybe talk about why that approval is important and sort of how it de-risked the path to the subcutaneous induction approval next year. Yes, it's really important because, and I'll start with the fact that LEQEMBI is an anti-amyloid therapy. Really, we believe the only one with a dual mechanism of action because not only does it target aggregated amyloid plaque, but it also targets soluble amyloid species. With that, we were able to make the case, and we have now in our U.S. label the need to treat or the option to treat intravenous maintenance. We've shown data out to four years, very recently at AIC, three years before, recently four years. What we see is that patients who continue to get LEQEMBI, either once monthly or intravenous or biweekly, actually differentiate from patients who are being followed in ADME and other cohorts. We see that they do tend to decline, but they don't decline as much. This is very meaningful at that early stage of disease. What we did was we were very systematic about it. This is, of course, in collaboration and partnership with our partner Eisai. We submitted for subcutaneous maintenance as a first step, and we were able to get approval for that. This is very exciting because now patients actually have the optionality to transition from intravenous to subcutaneous autoinjector. As I said, it could be at home, it could be in the clinic, and it can transition from intravenous. You could be on intravenous and then transition to subcutaneous. We've already shown data on bioequivalence on the 500 milligrams initiation dose, and that is what we've started our filing. This is a rolling submission, and it's an sNDA, sBLA to our subcutaneous filing, maintenance filing. We expect to hear sometime mid next year. If that comes through, then, you know, it'll really be exciting because I think it gives the patients and HCPs an opportunity to start at home. Great, great. You also have a TAU ASO in phase two with the CELIA study, which I believe is going to read out middle of next year. Maybe could you talk about what you're hoping to see in that study and more broadly how you see TAU fitting into the treatment landscape? Yes. As we know for Alzheimer's disease, two proteins are really pathognomonic and they are thought to be interconnected, actually. We know that TAU is important, especially as symptoms initiate right before that. This is an important area of query, scientific query. I think that we ourselves have shown that targeting extracellular TAU actually does not lead to any clinical benefit and even does not impact the tangles. We now know the tangles to be intracellular. The way we've approached this is we've approached this through a modality of antisense oligonucleotide. That is what BIIB080 is. It's an ASO. It's delivered intrathecally. We did a very small phase 1b trial. What we observed in that trial, a small number of patients, but it was an important observation that we were actually able to reduce TAU by 50 to 60%. We were able to see an impact on TAU tangles, which is what TAU PET shows, but also TAU fluid biomarkers and emerging signs of some clinical benefit. We have designed the CELIA study as the important next stage in this development where we can really have the scientific query be answered on if you reduce all form, all six isoforms of TAU, what is the impact on TAU, both fluid and PET biomarkers, but also is there an impact on clinical benefit? That is what we hope to see. Now we are testing three doses and two frequencies. We have the quarterly, but we also have the six monthly intrathecal delivery. That's important. We'll see a readout mid next year. We'll see what the trial shows us. Looking forward to it. Any interest in working on a subcutaneous version for that, and maybe speak to what's the feedback from the trial in terms of intrathecal dosing? Yeah, the feedback from the trial, maybe start there first, was very encouraging because actually the trial was enrolled quite rapidly. We are excited about that aspect. I think that we are definitely looking at tissue delivery mechanisms and more efficient ways of tissue delivery early in research and late in research. We are looking at shuttles, we are looking at other forms, other modalities. It is a very important priority area that we are focusing on. Great. For the GLP-1 trial in Alzheimer's, there's some debate on how which way that cuts for amyloid targeted therapies. Maybe you could share any thoughts there. Yeah, it's an important area. I would say that, you know, maybe just to back up, GLP-1s, I think that the reason, you know, there were some failures in phase 2. These were different programs. This is, of course, Novo Nordisk with Evoque and Evoque Plus with semaglutide. I think what's important here is the hypothesis is that addressing neuroinflammatory pathways could have an impact in Alzheimer's. The hypothesis is based on meta-analysis that was dementia of all causes and then, you know, further refined. It showed some benefit in the meta-analysis. I think that regardless of the outcome, it is a very important area. Number one, GLP-1s are really being widely prescribed. The fact that these trials are being run for early Alzheimer's disease gives and creates more awareness. One of the areas that we have been really thinking forward towards is how does this market expand? I think market expands with competitors. This is a very large space with newer patient populations as pre-symptomatic populations, but also with newer ways in which you could tackle other pathways that may be relevant. I think that's number one, that we think it will be, it's positive because it's already creating some increased awareness. The second thing is I think that we'll see what the data shows. In their trial, they actually used anti-amyloid as a backbone. We think that is important and is relevant and is the right approach because we don't expect that the GLP-1s will directly target amyloid. Even if this is positive, we think this could go into a space of combination therapy where tackling the anti-amyloid will be important in addition to potentially any benefit that we might see. We think net-net, it's a positive. Of course, we have to wait to see the data. We look forward to the data. Great, great. Another trial that there's a lot of interest in is Lilly's Trailblazer ALZ-3 and sort of what that could mean for your AHEAD 3, 4, 5. Maybe if we could just start with key differences in those trials, you know, why you designed your trial the way that you did. If you want to share any comments on what investors should read through when we see those results. Yeah, sure. I think just stepping back, as the world has been focused on longevity, we think that Alzheimer's disease, both early and pre-symptomatic stages, will be really important. In fact, we think pre-symptomatic is going to be a very large opportunity. It is with this sort of data and landscape in mind on how we think this will evolve that we embarked upon the AHEAD 3, 4, 5 trial with Eisai as our collaborators. We are really trying to address the landmark questions that are relevant for the pre-symptomatic, preclinical stage of Alzheimer's disease. Number one, and this is two trials, AHEAD 3 and AHEAD 4, 5. AHEAD 3 is aiming to answer the question that if you have 40 centiloids of amyloid in your brain, can we prevent further accumulation? What we know well is that it's a cascade. Amyloid continues to aggregate, then you have tau, and then you have symptoms. That's the first question. That's AHEAD 3 that has a biomarker endpoint, which is further accumulation of amyloid, so it's amyloid PET. AHEAD 4, 5 is tackling a slightly different question, which is, okay, you've now accumulated amyloid beyond the 40 centiloids. You may be at 60, 70, and this can vary at what point patients will have cognitive decline. Can we prevent symptom onset and cognitive decline? That is how we've designed the two trials. That second trial, the 4, 5, is the larger of the two. It is a more important question, I think, to answer because of the way patients are being diagnosed today. This could change in the future. That has a primary endpoint that is a sensitive preclinical Alzheimer's disease composite endpoint. It's the PAC-5, but it also measures amyloid and biomarker as a secondary endpoint. I think both are going to be really, really important. Now, with this in mind, when we screen patients, we use amyloid PET. We'll be looking at that at certain frequency. We also incorporated blood-based biomarkers to reduce screen failures. All of these efforts were really successful. I think what's important here is to be able to answer those two questions because you can think of the pre-symptomatic population as being stratified. As we get deeper into blood-based biomarkers, we may have more amyloid leveling biomarkers. We're not there yet, but we could have those. That would be a very important aspect. We've already tried to incorporate some of the early aspects of this. Now, the way that our competitor has gone after it is they are looking at can they slow down the progression to the next stage of Alzheimer's. With that in mind, I think their inclusion criteria ended up including patients who are CDR global score different from some of the boxes. So GS, CDR GS 0.5 and some 1. That's a big chunk of patients. That means they're already sort of symptomatic. I would wait to see, and I'm curious to see what they read out and whether they do a subgroup analysis that answers the true pre-symptomatic population. We're looking forward to our AHEAD 3, 4, 5 trial. We think that's the trial, and those are the answers that communities and patients and regular leaders will be looking for. Great. Maybe we can move over to SMA. You've got a couple of sort of efforts ongoing there with the high dose and also with Salinursin. Maybe if we could just sort of start with the unmet needs you see in SMA today and how that maps to Biogen's strategy there. Yes. I think this is an area of deep pride and success at Biogen. We believe it's going to be a very important franchise that can endure. The reason for that is we launched SPINRAZA and had approval in the 2016-2017 timeframe. It was the first disease-modifying therapy. It is still really, really important today. Despite the advent of small molecule as well as gene therapy, we know there's a residual high unmet need. This is clear. There are many important reasons for that. We have continued to build out what we think is going to be the next important step. With that, we did the DEBOT study for SPINRAZA high dose. The reason for that was we went with the right dose we thought was at the time. We believe based on pharmacology metrics, pharmacometrics modeling, that a higher dose was possible. When we did the DEBOT trial and the pivotal part B trial where we had symptomatic children with SPINRAZA naive, we saw an important drop in neurofilament. We saw that translate into motor milestones. We compared this to a matched control from the standard dose. In the part C, we actually transitioned patients from standard to high dose. We believe this was a very important trial. We filed for this. We were in review. Yesterday, we got a complete response letter. The important aspect here to note is that the complete response letter is not focused on any deficiencies in the clinical data package. It is actually related to CMC module 3 and to technical specifications. The FDA offered us options in their CRL letter to actually resolve them. The good news here is that we believe we have the data readily available to submit, resubmit. This will be a resubmission. We believe that will happen really soon in weeks. I'll move on. I think that the high dose is attempting to really address the high unmet need, outstanding unmet need. Now I'm going to bridge that because we haven't stopped there. We have a follow-on new molecular entity, also an antisense oligonucleotide, which preclinically we engineered and built with Ionis Pharmaceuticals with higher potency, durability, and stability with a potential once-year dosing. We recently actually declared proof of concept based on interim phase 1B data because we were looking at two doses. Now what's important to recognize here is our patient cohort with both the doses, the 40 milligrams and the 80 milligrams for Salinursin, as it's called, is really important because we chose in this trial to really go for the high bar. We chose previously treated patients, and then we dosed them with one dose of Salinursin because it's a once-a-year antisense oligonucleotide. We looked, we were looking for neurofilament light chains because we know that that's to be a reliable biomarker. Interestingly, we saw really exciting clinical anecdotal data from patients. I'll just quote one. We have a few, but I'll quote one, which is a child, a five-year-old who received gene therapy about the age of one, could not sit till the age of five, and then actually received one dose of Salinursin and was sitting a few months after. Very exciting. We have some several other vignettes, very similar. Now we're laser-focused on initiating our phase 3 trial, and I think we'll be able to initiate it in the first part of 2026. Excellent. I could ask you many more questions on both of those, but I want to make sure that we have time for lupus and also for Felsardimab. Maybe we could move over there. In lupus, you have Dapirolizumab pegol and litifilimab. You gave us a very thorough review of those just a few weeks back. Maybe before we get into the details of each drug, if you want to start by just sort of framing the opportunity in lupus that you see. Yes, I think it's a very critical question. If you step back and think about it, lupus is a very heterogeneous disease. If you saw our webinar, you heard us there saying, and you know, patients spoke at the webinar as well. Patients tell each other, "My lupus is not your lupus." That tends to go towards undertreatment and underdiagnosis. We have a statistic which is only about 20% of lupus patients are treated with one of the two biologics that are in the marketplace. While lupus is recognized as an entity and has been for many, many years, there are only two biologics that are available today. Dapirolizumab pegol (DAPI), which is one of our products, and we had a positive phase 3 trial. It's the third ever positive phase 3 trial in lupus, which is hard to imagine because it's a really important high unmet need. It also happens to be underserved populations. It's a very critical high unmet need. That, I think, is the big opportunity. We think this will need to be shaped, but we think that bringing therapies that matter to patients and to, from our market research, to KMEs and to providers will make the difference. We really believe that this is a very untapped market and bringing the right therapies will matter. Now we're going after it in two different ways. We have Dapirolizumab pegol (DAPI), of course, we're in our second phase 3 trial. Then we have litifilimab, which is tackling the type 1 interferon signature and really anti-BDCA2. We're tackling both CLE and SLE, CLE cutaneous lupus. We have three phase 3 trials that are ongoing. We are not stopping there. We have a phase 1 trial with lupus nephritis with Felsardimab. Two late-stage assets, one early-stage asset. As I mentioned, we just transitioned IRAK4. Lupus is very, very much within our indication selection possibility for IRAK4 as well. We're looking at breadth and depth. We're looking at different mechanisms of action. This is really based on our conviction that this is a very important market. Obviously, it's a large market. We need to expand it. We're not just waiting for data. We're taking a very different approach. With MS, we have a lot of experience in autoimmunity. We also have a lot of experience that you can have multiple products, all of whom could have a significant share. We don't think this will be a winner take all. We are already preparing for our potential lupus readouts, SLE, potentially end of next year in 2026, and then hopefully a cadence thereafter of CLE and Dapirolizumab pegol in years to follow. We are also working with our medical team, our providers, and building the education because these are all different mechanisms of action. We think lupus may be in the future ripe for sequential combination therapy. We are really thinking about a lot of these things. Great. I believe your next phase 3 for that will be litifilimab next year in SLE? Exactly. We have two phase 3s, and we are doing everything we can. We are excited because we're getting to the close of our recruitment. How would you frame what you're hoping to see in those data sets? Those data sets, you know, what's exciting about litifilimab is that we published in the New England Journal of Medicine, we published our LILAC study. We had two parts in that study. We had where we were going for patients who had manifestations of systemic lupus with fever, joint involvement, and all of that. Then we have cutaneous lupus. Really success in all of it. We think this will be a package. SRI4 is our primary endpoint for lupus, and then the class C for our CLE. We have a lot of secondary endpoints. It'll be a very robust look. With Dapirolizumab pegol, we're looking at BICLA. We're also looking at steroid sparing, which, you know, today's, you know, made its way into the guidelines because, you know, patients have a lot of steroids on board and we're seeing severe flare reduction. For litifilimab, I believe you're testing both the low and the high dose. What is the rationale for that? We had our one dose in LILAC, but we did a lot of modeling. We believe that while the low dose will work, we want to see if a high dose could work better. We're taking our lessons across drug development and trying to do it all so that we have the right answers at the time of approval. Great, great. For your Dapirolizumab pegol, the second phase 3 trial, I believe you've said 2027 to 2028 for that one? That's right. That's right. I noticed that you upsized that trial compared to the first phase 3. What were some of the considerations that you went into that? Yeah, I mean, we're very excited about the data that we had from our first phase 3. I think this is just making sure that we leave no stone unturned from having the right sized safety database. It is a new molecule, and we want to have that. Great. Yeah, it's an interesting market because on the one hand, as you said, there's only two approved drugs. There's limited uptake of those. On the other hand, it's fairly crowded in terms of the development landscape. Fast forward a few years, hopefully at least one of your drugs is on the market. Perhaps we'll see some competitors on the market as well. What would you expect to be the key differentiators for Biogen in lupus? Yeah, you know, I'm glad you brought up the point about being a crowded competitive landscape. It's an area where it's hard to recruit. I'm really proud of what the teams are doing because we've managed to do a really spectacular job despite COVID and all the geopolitical issues and the competitive landscape. I think that bodes well, that's helpful, right? It bodes well. The other piece I think that's important to remember here is that this is not a winner takes all. We think the market will expand. We think many therapies will be needed. We think it'll be like MS eventually, where there will be different mechanisms of action where patients may respond to one, not respond to the other. For example, with Dapirolizumab pegol, we recently shared data on fatigue. What we've heard from patients is that you're going after all these other endpoints, but what I can't really deal with is fatigue. We showed that we can really reduce that. Now it's another question of getting all of these things discussed with regulators and getting it into labels. I think these are very, very much differentiated. With SLE and CLE for litifilimab, they're going after type 1 interferon and anti-BDCA2. We think that, for example, with CLE, we think it's really a critical, it's a huge market. No real therapies out there for 70 years. Steroids that are the foundation of all these lupus manifestations are now in the guidelines as being steroids, like you have to get your patients off. The patients, when you ask them, they are looking to get off steroids. KMEs, prescribers are looking to get their patients off. They need an alternative that can match it on the endpoints and the treatment. I think that will be a differentiator. Great. Maybe we'll move to Felsardimab. You're pursuing several different indications here: AMR, IgAN, PMN, lupus nephritis. In one sense, they're all rare kidney, but they're also different in terms of unmet need, competition, so on. How do you think about the role that Felsardimab could play in those? Maybe your relative excitement across the three, the four at this point, yeah. Yeah, actually, more than four because MVI, that will start next year. It's very exciting, and we're looking at several other indications. I think Felsa is a really exciting space, and the way we've integrated the company, you know, very exciting, really exciting team that's leading that forward. We are excited because we started all three phase threes. That was a goal for 2025, and we're done, you know, with initiation. It's very exciting. Now, let me start with the fact that we believe that all these three are relevant indications where we've shown proof of concept. It goes back to my overarching principle that we don't take things into phase three till we show proof of concept. We've de-risked them to a great degree. I'll start with AMR, where we could get data as early as 2027. That's going to be exciting because today, if you think about patients and if you think about a societal burden, 75% of patients lose their kidney. They end up getting a rejection due to late AMR, and that is exactly where we saw transformational efficacy in a small trial, but really transformational efficacy. We believe that this is going to be really important, and it's driven by the anti-CD38 sort of autoantibody play. We think that's going to be really relevant. I think that from an AMR perspective, it's very exciting. We think that it's going to be important because the CD38 that's expressed on plasma cells, but we also think natural killer cells have a very important role to play, which may have been the reason some other products have failed because they weren't really targeting the key cell types that are relevant for this very important condition. Moving on to IgAN, you're right, it's very crowded. I think what the beauty of IgAN and the MOA here is, you know, it's this four-hit hypothesis where we think it's galactose-deficient IgA that's relevant for the mechanism. It's the autoantibodies to that. They form the immune complexes, and they get settled in the kidney. What we saw that was interesting to us, even when we did the diligence, and of course, the HiBio team has published on this, what we saw is that the proteinuria, the IgA reduction coincides with the proteinuria and impact on eGFR. We saw the durability 18 months after the nine-dose, five-month regimen was dosed. Now, it was a small trial, right, because many, many doses were tried. We see that there's stabilization versus placebo. That is very important because there's a potential based on market research that we've done. There's quite a significant potential on patients being able to have a non-chronic therapy. We think that's going to be relevant while maintaining the efficacy relevant to the April and the BAPs. It is an area of deep, continuous education and all of that. That is why we have really stepped up on our pre-market approval education and efforts on immunology. That encompasses rare kidney, but also lupus and all of that. Great. You preempted my question on AMR and why CD38 is a better mechanism. Maybe I'll move over to IgAN. You get some questions around, the UPCR stays depressed, but then it looks like the GFR is starting to trend lower a little bit. What gives you kind of the confidence that it's the UPCR, that that signal is what you should rely on and strategically, you know, you're comfortable going forward with this dosing holiday strategy? Yeah, I think the first and foremost is, I'll just say the main thing is that we saw the reduction in IgA. That coincided with the reduction in proteinuria and EGFR. The other piece here is that post-dosing, we saw the stabilization. The stabilization gives us quite a bit of confidence. We always have the opportunity to explore other paradigms. I think that this was a significant time off drug, and that was quite compelling. We've also done a lot of market research, and that is the response that we also get from those angles. Great. PMN, we haven't talked about that one yet. Very important. I mean, you know, I think what we've seen is that the refractory patients, the relapsed patients do really well. Now the way we've designed our phase 3 is that we think that the high-risk patients with the high levels of circulating PLA2R antibodies, but also patients who don't have that, can potentially benefit. We are expanding that base. We also know that more than one-third of the patients today do not respond to the anti-CD20s. We think this is a very large opportunity, 36,000 patients in the U.S., and one-third of those do not respond to anti-CD20s. That is the way we've designed the trial. We have confidence that we're going to see this movement and response in this broader population. We are really going after the broader population, not just the refractory and the relapsed population, also treatment-naive high-risk populations. Got it. IRAK4, you've mentioned this a few times. Maybe let's just give it this kind of center stage if you want to talk about that program and what the development plan would be for that. Yeah, right now, I think we're very excited. IND is accepted. We're about to dose our first patient. We're very excited. We're moving very fast. The first in human trial, which will be normal healthy volunteers, will give us the right data set to really expand. I think that Biogen, as it looks at expanding into immunology, is looking, and you know, we're doing with Felsardimab, you will see us considering the portfolio in a pill more and more. IRAK4, I think, will take center stage as we kind of contemplate that. It's more than contemplate because we've already started building out what a potential phase 2 program could look like. That's the beauty, I think, of targeting such a critical node in the inflammatory pathway like IRAK4, that it gives us the opportunity. We'll have the good problem of thinking of choices. We may choose more than one, like we have with Felsardimab. Great. We look forward to learning more on that one. Sure. We've covered a lot of different programs today. Would you like to maybe share some concluding thoughts on how all of these fit together into the kind of the coherent Biogen R&D strategy? Yeah, first, thanks so much, Will, for great questions here. I think stepping back, Biogen is at a very different point in many, many ways. One is our new launches are outpacing the decline of the MS portfolio, which is obviously a question. We think we're addressing that really well. The Alzheimer's franchise is continuing to grow, and we believe we have a differentiated asset. We think we're in the early stages. We are continuing to build a lot of depth in our lupus franchise, and as I spoke to, we have multiple shots and multiple mechanisms of action that we're targeting. Felsardimab is bringing our immunology, rare nephrology into the sort of forefront. We are already enrolled in all the phase 3 trials, and we continue to build on our expertise in neurology. You saw that with Salinursin, but also with Zorobinursin that has the potential to read out in 2027 in Dravet syndrome. Very exciting. We have just changed the shape, nature, look, and confidence in the aggregate profile of the pipeline today, but also of the individual programs. Any one of the individual programs we believe is very high value, potentially $1 billion or more. If more than one comes to fruition, that exponentially increases the value of the pipeline. We remain focused and disciplined on augmenting the pipeline with external and internal innovation, with the research, reinvigoration, and reimagination of open innovation. We're really tackling it from all sides while being very, very careful and disciplined about cost. I think I'm really excited about what we've been able to do and what the future could bring. Wonderful. Thank you so much for coming. Thank you. Thank you for having me.