 Yes, thank you, John. Difficult task because only 3% of you do use BVSTMAB. So I think you are all wrong. And I'm going to try to show you why you should use more BVSTMAB in your practice. And I always say, if I had a kidney cancer with metastatic disease, I would probably start my treatment with BVSTMAB. And I think that's what I would do. So when you look at NCCN guidelines, I think we have three recommendations which are in the same level. And the question for me is why not to use BVSTMAB? And the question is, I think, mainly because you don't know the drug. So what do we know? I mean, we know that VGF inhibition is key in RCC. And BVSTMAB is certainly the most specific VGF inhibitor with safety and toxicity only related to VGF inhibition with this drug. And Manuel, I give an excellent talk at Esmo recently showing that we don't know anything about the activity of the other targets and VGF. So probably, I mean, what we want to do is to target VGF. And what we do with TKI, we use dirty drug. So of course, VGF inhibition with this drug is the main driver for efficacy. But all the other targets we use produce toxicity. And we know all this toxicity. We know about hand food syndrome. We know about change in hair color, which is sometimes not trivial. And for me, it's very important because with this drug, you are not able to appreciate good wines. That's finished for you. So why should we use this drug? And the question is, why do we miss a good target? And we know that it's very dangerous when you use a target to miss the good target. And that's something that a lot of people know about that. So we have to use VGF as a good target. So one of the reasons why probably you don't use Bersimab is because interferon adds toxicity. And there is no question. I mean, interferon adds some toxicity, especially at the beginning of treatment. The good thing, and if you look at literature, is that when toxicity occurs, it's very manageable with those reduction. And in the other trial, we did those reduce. And what we showed is that with those reduction, we have very rapid improvement of the toxicity. No question here. And in addition to that, those patients where we add to those reduce are the better overall survival at the end of the patient where we don't have to those reduce. So toxicity with interferon is probably related to some more efficacy. And I don't think we have to be afraid by this toxicity with interferon here. So probably another argument is that Bersimab is expensive. And that's probably true. Bersimab is expensive. That's probably one reason why many countries have not to prove the drug. But if you look at the other end trial, I mean, most of the patients have stopped Bersimab at one year. And we still have an overall survival in the PFS, which is very significant. So if you put all these together, at the end, I mean, the cost of the drug is not so expensive, considering the benefits that you will get with this drug here. So why should I use Bersimab? I think Bersimab, first of all, is active. So this is the pivotal trial which led to registration in Europe, so called the avalanche trial that we did in Europe. It's now, I mean, seven years ago, that we published the paper in the Lancet. And when you look at the data, I mean, Bersimab with interferon produced a 10.2-month PFS. So remember what was in the compass trial. I mean, it's less than 10.2 months. So we are going to tell me, I mean, that's such a single trial. Why are you so sure that it works? It's not sure that we have less evidence with TKI. So Camilo showed a lot of patients treated with Sunitinib. I think we have a lot of evidence that Bersimab with interferon is active. So first of all, we have two large phase-free. And both myself and Brian, who is in the audience, I mean, conducted two large phase-free, showing that Bersimab is active in combination with interferon, much better than interferon alone. We also had a very recent phase-free. We've gained a large number of patients that Brian published recently called the Interact Trial where the control arm of Bersimab with interferon showing still a large activity of the drug. And this is what we showed in this study. 9.3 months PFS for interferon plus Bersimab in nowadays atmosphere. So still a very active regimen here. And then you would tell me, I mean, how could I think that it's better than Sunitinib? I don't know if it's better than Sunitinib, but at least in the only randomized study where we did compare the two drugs. I mean, Bersimab has been better than Sunitinib. So this was, of course, not the goal of this study. It's, of course, a randomized phase two. But still, I mean, in the studies that we did in France, called the Toravatrium, where the goal was to look at the time-serial in this Bersimab combination, we had two control arms, Sunitinib and Bersimab and Bersimab plus interferon. And when we look at the data here, that's what came out. So Bersimab plus interferon in this study was 16.8 months while Sunitinib was 8.2 months. So it certainly doesn't mean that Bersimab is much better than Sunitinib, but at least there are some patients where it's better. And in this study, it was better for patients who received Bersimab plus interferon here. So do you think it's only in one study that we have this kind of results? The answer is no. I mean, I like this study, which was recently published by Melisha, 147 patients in a large phase two. Bersimab plus lodos interferon, 15.6 months PFS. Never seen such a PFS in 150 patients. So think about, I mean, this combination and think about you have a kidney cancer. Why should not you use this combination for you? Overall survival exceeding 30 months. Of course, it's not one of my study and that certainly is a pity of the study, but it's a very convincing evidence that this combination is very active in kidney cancer. So let's look at what we have for Bersimab plus interferon. So these are all the trials we have with these drugs, Bersimab plus interferon, nine million three times a week plus Bersimab 10 milligram every two weeks. And you can see that the number of patients is quite high, 1,300 patients treated in these different phase three. Almost 10 months PFS on a consistent manner in this way with this drug here. And then if we add lodos interferon, maybe even Bersimab alone, as you have seen in the best trials that David McDermott reported at ASCOGU, I mean, it's still a very consistent and active drug in this setting here. So which is the ideal patient to receive Bersimab plus interferon? I think probably almost every patient could be a good candidate. So certainly patients with more indolent disease are excellent candidate. And every patient where you think that interferon could be a good treatment, I think adding Bersimab will have some efficacy and might be very beneficial for your patients. But I think if you look at intermediaries group patients, it's still very beneficial to give Bersimab plus interferon. So that was in Viavorant trials, the intermediaries group patient. And you can see that the hazard ratio is very high in comparison with Bersimab, 10.2 months compared with 4.5 months just in the intermediaries group patients here. So no question I think, I mean, this regimen is also active in intermediaries group, not only in good risk group, as people think it might be here. So that are the subgroup analysis for overall survival in Viavorant trial. And you can see that almost every subgroup that we have looked at in this forest plot benefit from combination with interferon plus Bersimab. So the only one which is very underrepresented in this study is the poorest group patients I would never recommend to use Bersimab as interferon in poorest group patients. And but in the first patients that John presented, I certainly would have selected Bersimab as the best treatment to give. So second point I think we are concerned about is patient with liver meds. And in this analysis here that you can see on the bottom of the slide here, those patients who have liver meds, at least in an exploratory analysis we did in Viavorant trial, seem not to benefit so well from Bersimab as interferon. So I would certainly be a little cautious by using the drug in patients with bulky disease and liver meds. And when you look at the median overall survival in patient without liver meds, it's very significant with liver meds it's much less significant here. So I would be very cautious about using the drug as first choice in liver meds patient here. So if I had to conclude my talk, I think Bersimab targets specifically VGF pathway. And I think that what we want to do in kidney cancer. So I think there is no reason not to use this drug because that probably is the best drug to inhibit VGF here. Bersimab is interferon has demonstrated consistently in many studies efficacy, at least as good as TKI, no question here. Bersimab is interferon is easily manageable. Of course I mean you have to deal with IV injection and with three times a week injection sub-Q. It's very easy to teach patients to do their own administration of interferon. We do much difficult thing in cancer actually here. I think Bersimab could be offered almost to every patient. And I think it's certainly a good choice if you can do that. And finally I think Bersimab is very convenient for your patients. And question here is when you use TKI, I mean you will have a lot of phone calls and we all know how difficult it is to deal with TKI and many of us are trying to set up, I mean phone conversation with other patients. And just with Bersimab is completely different and I know that Tom Hudson will be happy because then when you use Bersimab they meet your nurses and that my nurse is in Gustavo C and then I think it's very convincing that you should use Bersimab. Thank you very much.