 I think this is kind of combined looking at two angles. One is the understanding that we need to concentrate not just on saving these patients that are relapsing and relapsing after a long time, but also for these newly diagnosed patients if we concentrate our power, giving them a very effective treatment. Again, talking about dartumab and now another trial with isotuximab which is another new anti-CD38 antibody. So combining them with the standard of care, bortesumib, Revlimid, and dexamethasone VRD treatment, combining these four drugs together gets excellent results. We have a long time, we have the isotuximab showing very nice results in terms of minimal residual disease. So most patients over 50% of patients will achieve minimal residual disease a long time with the combination. And same goes with dartumab now in two years of follow-up of the Griffin trial where we've seen extremely deep responses already and now they're only deepening a long time as you give dartumab and linoleumid maintenance a long time. So patients will have more and more deep responses which will translate into very long progression-free survival meaning that the disease will not come back in many years in these patients. So this is very important in first leg. In advanced line, I think we're going over really a revolution in way we've seen the long-term results of the CAR T-cell trial. So we have the cartitude and the bluebird trials which are showing very prolonged duration of responses for patients. And most patients, I mean, in one trial over 70% with very advanced patients over six lines or seven lines of treatment and with both technologies where you take the T-cells and you re-educate against BCMA to target these very resistant plasma cells, even these very heavily predicted patients achieve very deep responses. And the nice thing about it is it seems that they're becoming very prolonged responses. And to that we add the newly bi-specific antibodies. So there are multiple trials now ongoing showing prolonged responses and very deep responses with these antibodies. They mimic the CAR T in a way. So one side of the antibody will bind the immune system and the other side will bind plasma cells and they bring the immune system with the plasma cells. So together this will cause the immune system to destroy the plasma cells. And again, we see very high response rate. And now after a year or two years of follow-up many patients stay in remission. And this is very amazing for very advanced patients. And to that we had other antibodies like Bellantoma which there are trials showing a way to make it better and maybe new image that are coming now. There is a, it's called cell modes. It's not ever called any more image. It's the next generation pomalidomide called the beridomide showing very nice responses. So in a way the future of myeloma in the next few years is going to be very bright. Things are changing, responses are better side effects are less. I think there's a very good perspective. Atash, we had two major talks about ALMA-loidosis. The one is the follow-up of the Andromeda clinical trial. The Andromeda clinical trials trial where newly diagnosed patients were randomized to receive either the standard of care treatment which is Bortesomy, cyclophosphamide and dexamethasone which most patients will know and recognizes the regimen that most patients receive to the same regimen plus the addition of dartumumab which is a new drug. Actually by now it's been going for a while and it's given as a subcutaneous fixed dose and to see both the safety and efficacy of the addition of dartumumab is first line dartumus in antibody which targets the plasma cells. So the whole regimen idea is to lower the amount of secreted amyloidogenic light chains as fast as possible and as deep as possible in order to regain organ function. So the main idea was to get to the hematologic response which is complete response. This is what we really want with the patients in order to achieve these goals of either better survival benefits and saving their organs which are damaged by these amyloidogenic light chains which are secreted by the plasma cells. So what we can see what we already know and have seen in the initial results of the atromeda trial, what the patients receiving the dartumab on top of the Bortesomy Velcade cyclophosphamide dexamethasone treatment managed to achieve a much better results in terms of achieving a complete remission. And this did not initially translate into survival benefit in terms because patients who do bad will do bad no matter what they get but most patients did well in both arms. However, those got the dartumumab has achieved maybe three times better results a long time and now after two years of follow-up we can see that these patients who are getting these deep results mostly the patients who are getting dartumab managed to achieve better organ responses meaning that their hearts work better and their kidneys work better even after half a year and much more than that a long time. So over half the patients have recovered their organ functions along two years of follow-up especially when they got the dartumumab. And this has led to assigning now in the United States and close now by in Europe as well the dartumab in first line in conjunction with Bortesomy cyclophosphamide dexamethasone for treatment of AL patients. And this is probably the first regiment that is being registered ever for a LMA-L8 dosis which is very much different from the treatments given up till now which are really taken from the myeloma world. So this is the first abstract which I think is very important to talk about. The other abstract which is also very interesting and has kind of a follow-up over the new antibody to dissolve the amyloidogenic material that accumulates in the organs mostly the heart and the kidney. The antibody is called Kale 101. It is a monoclonal antibody which was manufactured to recognize the kappa or the lambda light chains which are sedimenting in the organs and to remove them from the organs. So this phase one two study managed to give this antibody once every two weeks. And the good thing about it is that patients had very limited side effects. So there weren't too many side effects when the patient got them. Not a lot of patients but these patients who got it had heart involvement and kidney involvement. And the amazing thing about it is that almost all patients or significant amount of them has responded in terms of getting their organs function better. Both cardiac patients and kidney patients where the protein secreted in the urine was lessening a long time. Same goes for heart function as measured by probian P levels which were getting better a long time. So in general there is hope and this monoclonal antibody is now being tested in a very large clinical trial worldwide in newly diagnosed patients again with bortezomib cyclophosphamide dexamethasone or with dartuma bortezomib cyclophosphamide dexamethasone. So these are two very good news for amyloidosis patients. As I was showing, it was approved for a reason because dartuma was shown very nice results especially a long time in these patients making them rendering them with better organ function a long time which is really something that we were missing even in large clinical trials. And the next drug that we hope will come into treatment in amyloidosis patients is certainly the one that I was talking about the Kale-1-1 because this is a hope to target the amyloid from the other side instead of targeting the manufacturing of the amyloidogenic light chains it targets the sediment, the end point result of a amyloidosis, the sedimentation of these light chains in the organs. So when we are talking about a way to prevent amyloid from becoming amyloid and to stop the toxicity of these light chains over the organs now there will be another way to maybe remove it from the organs and a long time both combined together probably will bring much results to these very sick patients. Currently, in most patients we will be using a Bortezumi-based protocol in first line usually combined with chemotherapy patients with amyloid do not unlike myeloma patients do not tolerate very well than Alidomai or Revlimid which is used in many myeloma patients in first line. So most patients will receive this protocol Bortezumi-based, my dexamethasone probably in the near future, there are two mob will be added to it. For relapsing patients, we have other medications we do use the image mostly Revlimid but which is sometimes very difficult to take so many patients will be switched to Promalidomide which is much better tolerated a long time and in the near future, well hopefully we'll see other technologies emerging from myeloma treatment like Belantamab which targets PCMA it's another molecule on the plasma cells over the CD38 that is now being targeted and may show many hopes in myeloma patients probably it will be effective as well for amyloid dosage patients another new molecule which is emerging is Venetoclax most patients with amyloid over 50% of them mostly over 50% of them will harbor translocation in their cells of the chromosomes 11 and 14 and for some reason this fusion protein that becomes of this translocation is very sensitive to a new medication called Venetoclax we have lots of experience with Venetoclax and leukemias chronic and acute leukemias however it is very, very effective in these 11, 14 patients with myeloma and probably with amyloid as well so maybe in the future this will become another very important drug in amyloid dosage treatment.