Hello, welcome to the IL-15 vitiligo phase I-B 24-week efficacy results conference call. My name is Alex. I'll be coordinating today's call. If you'd like to ask a question at the end of the presentation, please press star followed by one on your telephone keypad. I'll now hand it over to Chris Stevo, SVP, Investor Relations. Please go ahead. Thanks, Alex. Good morning, good afternoon, everyone. Before I turn the call over to our CEO, Richard Francis, I want to remind everyone that we'll be making forward-looking statements on this call. The company cautions investors that any forward-looking statement involves risks and uncertainties and is not a guarantee of future performance. Actual results may differ materially from those expressed or implied in the forward-looking statements due to a variety of factors. These factors are described in our earnings press release and our most recent 10-Q and 10-K filed with the SEC. Any statements we make are only as of today, and we undertake no obligation to update these statements subsequently. With that, Richard Francis. Thanks, Chris. Good morning, good afternoon. Thank you everybody for joining the call. Today, I'm very excited to share with you our anti-IL-15 vitiligo phase I-B 24-week efficacy results. Today, joining me on the call is Dr. Eric Hughes, Head of R&D and Chief Medical Officer, who will go through the details of the results. Then at the end, we'll have a Q&A to answer your questions. The slide you see up today is very exciting and a milestone on our Pivot to Growth journey, as this slide highlights the progress we've made in transforming Teva into a world-leading biopharma company. As you see by what's in front of you on this slide, that 2026 is a year of milestones. Originally, we had expected seven, but with the addition of ecopipam's NDA filing, we now have eight key events expected this year. In that context, I'm really proud to talk about today's anti-IL-15 phase I-B results in vitiligo. I remind you, besides today's news, we have already shared the duvakitug maintenance data for UC and CD in phase II in February. We also acquired ecopipam and filed it with the FDA a few weeks ago. I'd like to remind you there are many more milestones coming up in the second half of this year with phase IIa top-line results for celiac for IL-15. DARI will have its pivotal phase III readout. Then for emricasan, a futility analysis of the phase II. I'm also excited about potential tomalanzapine at the end of this year. Then finally, we have the anti-PD-1/IL-2 data coming up right at the end. A lot of exciting data coming out from our innovative pipeline. Really key year as we transition to a world-class biopharma company. If we go on to the next slide, the reason why this is really important to create value and sustainability for Teva is if you look across this pipeline from olanzapine to ecopipam to DARI to duvakitug to emricasan, to IL-15, all of these have the ability to be $1 billion products in their indications. In fact, any one of which could be transformational to Teva. As you can see by this slide, the size of the potential markets that they are entering into is significant and growing. Yet we have a high-quality pipeline that is well-positioned. We continue to drive our innovative portfolio for growth for many years to come. I do remind you that we expect our innovative portfolio to generate $3.5 billion of revenue in 2026. Everything on this slide will be building upon this already fastly growing platform. I'd also like to point out that two programs on this list, anti-IL-15 and TL1A duvakitug, will have multiple indications. For anti-IL-15, as I hand over to Eric, I know he'll talk to you about vitiligo data, but also talk to you the potential this product has in other indications. With that, I'll hand over to Eric. Great. Thank you, Richard. It's great to be here on the call today to talk about this exciting new data we have for our anti-IL-15 program. If we can have the first slide. Vitiligo is an important disease. It's an autoimmune disease that destroys the melanocytes because of an immune reaction. It's a pretty common disease. It's about 0.5%-2% of the global population. Many people are afflicted with this, and many are undiagnosed still. There is a psychological burden to the disease. It's not just a skin discoloration. It can cause anxiety, depression, and social isolation. The only FDA-approved treatment right now is a topical that covers less than 10% of the body surface area. What's really needed is new treatments that are systemic in nature to treat the whole body. Because it's not just the face, it's the entire body that can be affected. Come to the next slide. Why is IL-15 important? Well, it's a key cytokine in the pathogenesis of vitiligo. What happens is keratinocytes under stressful conditions, which are a number, can cause the secretion of IL-15. It's that IL-15 localized in the dermis itself that drives the production and residence of CD8-positive T lymphocytes that are cytotoxic, and they attack the melanocytes and destroy those cells that cause the pigment within the skin. With our antibody, blocking that IL-15 signal blocks the continued proliferation and resonance of these cells in the skin, which will impact the destruction of the melanocytes and potentially have the potential to be a disease-modifying treatment. It's very exciting biology and a real targeted therapy for vitiligo. Come to the next slide. What differentiates our anti-IL-15 antibody? Well, first, it's, we believe the most potent anti-IL-15 antibody out there. It was very well designed by our own labs at Teva. It's a Teva-born molecule. Same team that made duvakitug made this molecule. Its half-life is very long. It's a clinically relevant dosing. You can see that you have a 38-day half-life, which is very important when it comes to the convenience for patients. That 38-day half-life that you see on the left-hand side of this slide translates into strong target engagement that you see on the right-hand of this slide. This graph is showing the suppression of free IL-15 level in the serum. What you can see here is a remarkable target effect where rapid reduction below the limit of quantitation happens within one or two days. At the top dose, you can see here, there's suppression below the limit of quantitation out to 80 to 90 days. Clearly, with the half-life and the target engagement we see, the potential for dosing every quarter, that is once every three months, is a strong possibility for this molecule. We're very excited about the potential of a very easy-to-give, safe molecule that's a subcutaneous shot once a quarter. Go to the next slide. Let me do a little bit of a tutorial on how we measure. Go back one. Yeah, go back one. How we measure the VASI score. If we go back one more slide. Go back one slide. Forward one. Okay, well, I'll just start with this slide. Going over the study design. This was a proof-of-concept phase I-B study. It was a design where we give one dose at day zero and then one dose at week 12. Over a 24-week period, which is the endpoint of this study, we've only given two shots of the medication subcutaneously. It's looking at about 38 patients. We looked at VASI scores of both F-VASI and T-VASI. It's important to note that 66% of the patients in this study actually had skin involvement that was greater than 10% of their body. We'll be monitoring the subjects out to 80 weeks. A simple study looking at a conveniently given subcutaneous shot with an endpoint at 24 weeks. If I can go to the next slide. Here, going to this slide I was referring to before. Just a quick tutorial on how we look at and measure F-VASIs and T-VASIs. It's a fairly simple methodology, but it's actually very reproducible with our dermatologic investigators. When you look at the F-VASI, it's a simple measure of using your fingertip, looking at the number of areas or the surface area involved in the face. You use a fingertip, look at the areas of depigmentation, count up the number of fingertips, then multiply that by the level of involvement at each, going from zero where there's full pigmentation to 100% where there's no pigmentation. You multiply that and get a score. In a similar way, you do the T-VASI, which is using a hand, which is about 1% of your body surface area, you use the number of hand counts to quantitate the T-VASI, again, multiply it by the extent of involvement in those areas. That gets you these two scores. These are regulatory endpoints that can be used for a phase III study. Now if we go to the next slide. Getting to the exciting part, looking at the data that we saw in this study. Those patients with a facial VASI score from baseline to 24 weeks after just two shots of the treatment achieved a 42% response rate for F-VASI50. That's a 50% improvement in their facial score. And then the F-VASI75, where 75% of your face improves, those people, or about 21% of the population achieved that. And then with T-VASI, which is a 50% improvement of your total body, 7% achieved that. We're very happy with these results. This is very consistent with other phase II studies with other oral systemic treatments. For me, actually, the most interesting and satisfying fact was not only did we get these regulatory endpoints, but when you ask the patients what they thought their skin did during the study, the response was pretty impressive. With the facial Patient Global Impression of Change score, which is a validated score in vitiligo, 75% of the patients in the study said that their facial skin improved. And half of those were much to very much improved. And then when you look at the total Patient Global Impression of Change score, 55% of those patients said that their skin improved. I've done work in dermatology before. I think that the regulatory endpoints, we're glad to see we achieved a very competitive profile. It's even more important that a patient who's looking at their skin every day and thinks about this on a daily basis actually thought that their skin is perceived as improving was very impressive. We're very happy to see that. And I think that will drive a lot of patient satisfaction with a potential treatment in the future. Go to the next slide. How does this compare? One of the things that we've been mentioning is we wanted to be compared to systemic therapies. upadacitinib is an oral JAK therapy that it was actually just got a positive opinion from the CHMP, I think, just last week. When we look at the F-VASIs and the T-VASIs, compared to that at 24 weeks, I think that they're comparable, if not favorable. 42 compared to 38 and 39, for the facial VASI at 50. For the F-VASI75, we see a 21% versus 19% and 14%, and a T-VASI of 7% versus 6% and 11%. This is very encouraging, for what we think about the effect that we're seeing. And it's important to remember, our product is a shot once every quarter. And it has, to date, a favorable safety profile. When you compare that to an oral JAK that it has to be given each day and then has a certain, a black box warning in their label, we think this is a good value proposition for patients given the convenience and hopefully the safety that we show in the future. If I can go to the next slide. One thing we did for today, which I'm very thankful for, two of the patients in the study, they're not representative of everyone. These are two patients that said they had very much improved skin on their face. They were kind enough to consent and give us their permission to use the pictures from their baseline to their week 24 time point. What you can see first on the left-hand side, this woman had significant hypopigmentation, with a wide area of her face. You can see almost loss of pigmentation completely. At 24 weeks, you see a considerable improvement in that discoloration she had, particularly on her cheeks and her nose and above her brow. The gentleman on the right, similarly, with a slightly darker skin, saw clear repigmentation on the brow, around the nares, and around the mouth as well. This is pretty, to me, dramatic effects where you can see, even on a normal picture, the changes that you can see in the color of the skin. I think this can have a huge impact on a person's quality of life and all the troubles that they run through in their mind every day when they're looking in the mirror. We're very proud of that, and we're very happy that these people were kind enough to let us use their pictures today. Like I say, a picture is worth a thousand words. Really puts the numbers in perspective. Go to the next slide. One thing we think about is, what is the opportunity here? What's the level of unmet medical need we see in vitiligo? Today, before any systemic therapies are even available, we think there's about 4.1 million people in the U.S., EU, U.K., and Japan. The targeted group, the therapies that the patients will be targeted for is about 2.7 million. Currently, there's no approved treatment for that systemic therapy right now. It's important to note there's analogs in dermatology that really drive what we think will happen in the future. Psoriasis and atopic dermatitis are great examples where a disease area that was probably underappreciated 15 to 20 years ago, as safe and effective biologics came out, really drove the advance and the size and the understanding of the unmet medical needs. Psoriasis obviously grew to a very significant population. Same thing with atopic dermatitis. We think that there is the potential that as we have better therapies, like we hope we're developing here, we will drive the development of this market and really create a disease awareness when new therapies come out. We're excited by the future opportunities here. If we can have the last slide. Oh, I'm sorry. I did want to mention, too, anti-IL-15 is a very important cytokine, not only for vitiligo, but there's a lot of crossover and carry-through with other diseases, such as alopecia areata. We have evidence pre-clinically of atopic dermatitis, but also in gastroenterology, such as celiac disease and eosinophilic esophagitis. That reminds me that, remember, we'll have our proof of concept study in celiac disease readout in the second half of this year. There's a lot of great potential for anti-IL-15 therapy across multiple disease areas, and we're excited to be looking at those in the future. If I can have the next slide. We believe we have a differentiated product. This is an internally developed anti-IL-15. We believe it has the highest potency of the anti-IL-15s in development right now. It has a prolonged half-life of about 38 days, which will allow us convenient dosing every quarter, based on our data today and our target engagement biomarker data as well. I think the data today are encouraging. I think it's in line with the systemic therapies that have been also seen in phase II. We're moving forward with our phase II program this year. I also should mention that it's been very well tolerated. Really no safety signals seen to date, and we're very happy about that. We've already met with the FDA. I'm very happy to say that. We're now incorporating feedback from them into our phase II study, and we're very excited to get that going this year. As I mentioned, in the second half of this year, we'll also have the proof of concept data readout from our celiac study. We're excited in the future to be expanding into other indications that are a natural fit for anti-IL-15 therapy. With that, on the next slide, I'm going to pass it back to Chris, and we'll entertain questions if anyone has them. Thank you. Thanks, Eric. While Alex is preparing the queue for the Q&A, I'll just remind people that we should ask them to limit themselves to one question and one brief follow-up to allow us to take as many people's questions as possible. Of course, they can get back in the queue and ask another question. With that, Alex, please go ahead with the first question. Thank you. As a quick reminder, if you'd like to ask a question, please press star one on your telephone keypad, then we ask you to please pick up your handset to allow for optimum sound quality. Our first question for today comes from Dennis Ding of Jefferies. Your line is now open. Please go ahead. Hi, good morning. Thanks for taking my question. Just one for me. On the long-term follow-up data, do you expect a big rebound in IL-15 once you stop the drug like you saw in the PK study? How do you think that could manifest in safety? Given the durability of the IL-15 knockdown, curious if there's a plan to approach dosing differently for induction and maintenance, and if six-month dosing could be possible for maintenance. Thank you. Thank you, Dennis, for the question. First of all, I'll talk about the long-term follow-up. One of the things that our team has done, which I'm very proud of, they did extensive follow-up even of our phase I study. We took some of our phase I studies out to like 400 days, and we've actually characterized the suppression of IL-15 and then the recovery as well as other things like NK cells. We have a very good sense of the suppression level, the rebound, and then it comes back to baseline. There's no associated AEs with the rebound of the IL-15. In fact, that's really consistent with just the way in which the body recovers the homeostatic levels of NKs and the effects of IL-15. It all comes back to baseline, and we follow that out for a long period. That's exactly why we follow the patients in this study out to 80 weeks. We'll have a very good data set. I think the regulators appreciate long-term follow-up. We're confident in how the drug works and how the body responds to it. Now, you mentioned in your other question about, I believe in an induction dose and a maintenance dose. We're approaching this program with no induction dose. We are starting right off with a dose, and we're going to continue that way. I think that given the characteristics of the disease pathology, the loading dose is probably not necessary because I think we're shutting down the IL-15 within just a few days with the doses we're using, and that's probably not going to be necessary. Even in the fact that there's an exuberant expression within the skin, I think that the way that we're setting the program up is the most convenient for patients. Just the one subcutaneous shot and then continue that same shot every quarter. That convenience, I think the biology indicates that that's a good pathway to go. Thank you. Thank you. Our next question comes from Matt Dellatorre of Goldman Sachs. Your line's now open. Please go ahead. Great. Good morning, guys, and congrats on the positive data. First on efficacy. Clearly, the data compare favorably to the oral JAKs. I'm curious, maybe depending on what you were seeing in the early washout period, what you think you might be able to achieve on F-VASI75 at 48 weeks. It looks like RINVOQ did maybe 23%-25% on a non-adjusted basis, F-VASI75. Realize you guys just use a single dose here. Should we expect you to do further dose finding in phase IIb, or are you all happy with this specific dose? Thank you. Great. Thanks, Matt, for the question. Yes. Your first point, and you broke up a little bit there, so correct me if I got the question wrong, but I think your first question is what would you expect at 48 weeks. If you look at programs out there and the data that's been published and what our expectations are here, when you think about vitiligo and how the disease happens, T cells go in there and kill off the melanocytes. When you stop that destruction, the melanocytes have to then repopulate into the skin. Usually, they come back from germinal centers at the hair follicle. It takes time for these cells to come back and then recolor the skin. The reason I bring that up is that time is something that helps you. From 24 weeks to the 48 weeks, we do expect that we'll have to obviously test this, but we do expect the scores to increase. You've seen that in other phase II programs as well and phase III programs. That's expected. There is a time element to the recovery, I believe, in vitiligo. That's my answer for the 48 weeks. With dose finding, this was a proof-of-concept study. We looked at one dose. Of course, we will be doing a dose ranging study in our phase IIb, and then that will rapidly transform into a phase III study. One of the things that we're working on right now and have discussed with FDA is a seamless study design, which is a rapid way in which we can progress this compound quickly and use the known endpoints very efficiently. Thank you. Thank you. Our next question comes from Jason Gerberry of Bank of America. Your line is now open. Please go ahead. Hey, guys. Thanks for taking my question. Just wanted to follow up on the dose question. You outlined the PK/PD data in healthy volunteers, five doses and then show the two doses on the free IL-15 levels. Can you clarify which of those doses you studied in the phase I-B? Just kind of wanted to get a sense of are you leaving efficacy on the table and as you look at doses in phase II-B, have you studied that dose level 2 that appears to have the maximal free IL-15 suppression levels in this study? Or if that's planned to be evaluated in the subsequent phase II-B. Thanks. Thanks for the question, Jason. I can't tell you the dose today. That will be presented in the congresses for the proof-of-concept study. To your question about how do we approach phase II-B now, this is the proof-of-concept single dose. We will be doing dose ranging, and that's important because I frequently obsess around our modeling and simulation. There is dose optimization we can do for the dose between the data we have on our PK, the data we have on our free IL-15, and the data we have on our NK cell reduction. All those together, I think I'm pretty confident in how we're going to select the doses for phase II. Thank you. Okay. Our next question comes from David Amsellem of Piper Sandler. The line's now open. Please go ahead. Thanks. On the percentage of patients with total body surface area coverage of over 10%, I think you said it was that 66% of patients in the phase I-B that had over 10% coverage. What's your expectation or what should we expect regarding those patients in the phase II-B? Is it going to be all comers or is it going to be patients with over 10% BSA coverage? That's number one. Secondly, with that two-thirds, one-third mix in the phase I-B, how do you think that may have influenced the data on T-VASI and F-VASI that you had disclosed this morning? Thanks. Sure. I'll answer the last question first. We didn't see any effect on the baseline level on the efficacy. It was very similar across the board. Getting back to the question of what do you expect to come into a phase II-B study. When I look at the publications out there to date, looking at some of the studies have different baseline factors. In general, you see about 60%, 70% of the patients greater than 10% from what I see. When we design the phase II, it's going to be very clear. The baseline factors will include greater than 0.5 on the facial VASI plus greater than five on the total VASI. I think that's consistent with all phase III programs at this point and what I think is expected by regulators at this point. The population here reflected what we'll probably see in the future, and our baseline factors will be based on a 0.5 facial VASI with a five on the total VASI. Thank you. Thank you. Our next question comes from Louise Chen of Scotiabank. Your line is now open. Go ahead. Hi. Thank you for taking my questions, and congratulations on the data. I wanted to ask you if you think there are any read-throughs from your data today to your upcoming phase IIa celiac disease readout and any of the other products that you mentioned on page 16 of your presentation. I also wanted to ask you, is there an opportunity to combine your drug with other vitiligo drugs that are on the market? Thank you. Great. Louise, thank you for the question and comment. I'm just writing my notes down here. Louise, your first question on the read-through. I think most people in the field, when they look at vitiligo, they would say alopecia areata goes hand in hand with vitiligo. I would like to think that we have a decent shot when we do those studies, but it needs to be shown still. That's just a potential. I also think there's a read-through with celiac disease. IL-15 is a key cytokine when it comes to celiac disease. We have some great preclinical data in non-human primates. We have some great target engagement data. We had our first proof of concept in celiac patients where we showed fatty acid-binding proteins clearly differentiating between active and placebo. This second study that we'll read out at the second half of this year for proof of concept with the biopsies, I think hopefully will show similar effects. We still have to see the data. I do think there's quite a bit of read-through with these related diseases. In fact, many people who have vitiligo frequently have alopecia. People who have celiac disease frequently have vitiligo. There is a lot of crossovers, I believe, between the number of indications that we're looking at. Your other question was an interesting one about the use of combination therapies. That's a very interesting question. I don't know whether you could add a JAK to an IL-15. They're vastly different mechanisms. The exciting part about IL-15 is it's really potentially impacting the disease process itself. That is the T resident memory cells, where you're decreasing those and affecting them within the skin. That could be theoretically a prolonged effect. JAKs, for example, are much more immediate tamping down and a broad tamping down of the inflammatory response in the moment. That's a very interesting possibility. Theoretically, since they're such different mechanisms, you could do that. I think you'd have to prove the safety and efficacy. Potentially a more interesting possibility is there is a study out there where there was an anti-IL-15 that showed minimal activity in vitiligo, but with UVB light therapies, they showed a pretty dramatic effect, which scientifically might make sense because you're getting rid of the cells that are destroying the melanocytes, then you're adding that stimulus. This is purely speculation. There is some data out there that suggests that that might actually be something to study in the future. Thank you. Thank you. Our next question comes from Chris Schott of J.P. Morgan. Your line's now open. Please go ahead. Great. Thanks so much for the question. I just want to come back to the phase II celiac data. Can you help set some expectations here on what type of benefit you're hoping to see in that indication? When we start to think about maybe the broader suite of indications beyond vitiligo and celiac, is your plan to maybe fully de-risk these first two indications before you expand? Should we think about Teva starting to scale up some of those other indications that you lay out in slides kind of in parallel with these first two? Thanks so much. Thanks, Chris. Yeah, great question. The celiac study that will read out in the second half of this year is a study in approximately, I think it's about 50 patients. It's a placebo-controlled study. It's a gluten challenge proof of concept study. This is an important study to give us a sense of what effect are we actually having on the gut histology. In this study, we dose them with either placebo or active, then two weeks later-- and it's just a single dose. Two weeks later, we challenge them with eight weeks of a gluten diet. Then we do a biopsy at baseline, and then we do a biopsy at the end of the eight weeks. The important thing, as I mentioned, is to give us a sense of, are we affecting the gut lining when people are exposed to gluten? This is important because that will drive our understanding of the endpoint in our registrational studies, because that will likely be a combination of both the gut histology and a patient-reported outcome. The proof-of-concept study that we'll read out later this year in celiac disease is just that. It's somewhat of an artificial study, but it tells us whether we have a true effect on a very important outcome. That's an effect on the histology of the gut. I would level set everyone that we'll use whatever publications are out there to compare our effect on that crypt depth to villus height ratio. That's going to be the most important readout of that study. Your second question was, what are we thinking about other indications for this? I think that I have an order in my head. To me, it's vitiligo, celiac with alopecia areata, probably all going in simultaneous development. It's just a matter of speed, and that's what we're trying to do the best here at Teva is move very quickly. We'll do probably those three in parallel, and I think we're moving pretty quick on them right now. Thank you. Thank you. Our next question comes from Ash Verma of UBS. Your line's now open. Please go ahead. Hi. Good morning. This is Dee on behalf of Ash. One question. Do you see any notable difference between the active and stable vitiligo patients just in terms of response rates? Yeah, great question. We did look at that. We did have both active and stable. Just for everyone's knowledge, active is if they've had any change within the previous three months before the study. Stable is considered anything that hasn't changed in the previous three months before the study. We looked at that; they're very small numbers at this point when you start dividing up this study. Numerically, actually, the stable looked a little bit better than the active, that has to be studied in a greater sense in the future with bigger numbers. Actually, it was kind of encouraged by the fact that the stable looked slightly better. Thank you. Thank you. Our next question comes from Umer Raffat of Evercore ISI. Your line is now open. Please go ahead. Hi, guys. Thanks for taking my questions. I have a couple here, if I may, just to clarify some of the things you've mentioned, Eric. First, let me start off on some of these efficacy comparisons versus some of the JAK studies. The JAK studies were enrolling total VASI 5-plus, only if they had failed a topical steroid or it was active disease. I think you just touched on it, Eric, where some patients were stable, some were active. If they were stable, the JAK study enrolled 10-plus total VASI. Could you remind us, what% of patients were 10-plus, just so that we're looking at apples to apples when doing some of the comparisons, number one. Secondly, on dosing, from your experience so far, how are you thinking about whether it's serum IL-15 inhibition, which is the key driver, or whether NK reduction is a key driver? I ask because if it's IL-15, presumably you can get to deeper efficacy with monthly dosing, whereas if it's NK, which I suspect it may be, theoretically the PD lasts six months, it doesn't have to be quarterly. I'm just trying to understand quarterly, because it seems to me like either its monthly or it's every six months. I'd love to get your take on that. Yeah. Umer, thank you. Great question. The first one was who had greater than 10-plus on the%? Is that what you're asking in the study? Yeah. Was the vast majority of patients- I'm sorry, you broke up there, Umer. You can just repeat that again? Yeah, I'm sorry. I was just wondering, is it vast majority of patients that were 10+? It was 66% of the patients had greater than 10% of their body. It was a majority, and from what I look at the literature, that's usually what many of the phase II and phase III studies had enrolled before. Very similar to what we should see in the future. Your second question is actually super interesting, and I think it's a great one to speculate a little bit with you on. When I look at the data and I look at NK cell reduction, which you're correct, the NK cell reduction goes down, and it takes a number of weeks to months to recover back to baseline. The IL-15 is more rapid, and the IL-15 actually drives those effects on NK cells. When it comes to thinking about dose duration for vitiligo, remember, it's not necessarily the NK cells that are driving the pathology, it's the T cells, the resident memory T cells in the skin. I feel like I have to stick with determining a dosing based on the free IL-15 suppression, not the NK cell reduction, because I think the kinetics of the NK cell reduction may be true, but unrelated to what the effects are on the T cells. I have to go by the target engagement of the IL-15 that we measure in the serum. That's how I differentiate it. If you were to make a link between NK cells and actual vitiligo, you could potentially go longer, but I don't think that that's the way we're going to go forward now. We're going to base it on the 3-month suppression of free IL-15. I hope that answers your question. Sure. Maybe just more on a multi-dose basis, perhaps on a more frequent monthly or so, should we expect deeper efficacy if free IL-15 is the driver here? I certainly believe there's a potential that this is a disease-modifying treatment. Remember, this is not just a drug stopping an inflammatory process. It's stopping the signal that brings the T cells to the epidermis. If you're getting rid of the cell that's actually causing the disease, that could be a prolonged effect over time. If that's persistent, that would potentially have a greater and greater effect over time. We have to show this, but it's basically a completely different way of treating it in many ways. Thank you very much. Thanks, Umer. Thank you. At this time, we currently have no further questions, I'll hand it back to the management team for any final remarks. Thank you everybody for your interest today and calling in. Once again, just want to reiterate, we're excited about the progression we're making not only with anti-IL-15 in vitiligo, but the progress we're making on transforming Teva into a world-leading biopharma company. As I pointed out at the start, this is just the second of eight milestones this year. A lot more to come on this journey. Very exciting times. Once again, we appreciate your interest, the inquiry, but there's a lot more to come. I think keep your diaries free because there'll be more calls like this coming up. Thank you. This concludes today's conference call. Thank you all for joining. You may now disconnect your lines.