Hi there, I'm Faith Davis and I work in NYU Langone in New York. My name is Garris Morgan. I also work in NYU Langone in New York City. We've been to a very interesting meeting today here at the IMS meeting in Rio de Janeiro. It's a fascinating new look and summation of data about how to address high risk multiple mile owner. And I thought the discussions were fascinating and Faith here has been really key in developing the new definitions of this disease. Yeah, so we've had a number of meetings of world experts over the last couple of years. And we launched today the new IMS and IMWG definition of high risk. And so that has four key features. The first one is deletion of 17p. The second one is either a bioallelic deletion of 1p or an antifocation of 1p with a deletion of 1p. The third one is a translocation such as a 414, a 1416 or a 1420, but with a 1q and a 1p or 1p and or a 1q. And the last one is patients with normal renal failure and a high beta 2m. So there's a few subtleties and changes from the previous criteria. And one of these is the fact that we now are encouraging people to do mutation detection. So looking for mutations of 17p and as well as trying to pick up some of the smaller deletions in one way. And so that has a whole new set of challenges for laboratories moving forward. And I don't know if you want to talk about those things. Yeah, first of all, I'd like to say that this is a really important change. And although you may not think it's important as a patient, I think it's very important for patients to understand this, because there's a group of people out there that have been told they have high risk disease, who clearly don't have high risk disease based on the old definitions. And so really look at your own results, work out exactly what they mean for you, seek an opinion to help interpret it, talk to the people at Health Tree, they understand these things. So I think that's really going to be good news for a lot of people who's worried that their disease is going to run out of control and not respond. But we know that with new good treatments, people with some of the old factors are doing perfectly well and getting long, durable remission. So important point number one. And then talking about the future, we have to have better ways of detecting these abnormalities in the clinic. We used to use FISH, as Faith pointed out. But what we need to do going forward is to use these new whole genome technologies and take advantage of AI, high throughput processing of data to rip out the important prognostic variables. Then we can add new things in, such as APEBX signatures, different mutational groups. All of these things are going to transform the future. And we'll start to see a new generation of abnormalities that predict response to these newer treatments like CAR-T and bispecifics. And it was really exciting because after talking about the definition of high risk, we were fortunate to hear a number of talks that people were giving about how high risk patients are now responding to treatment and the importance of treating these patients very carefully and monitoring them very closely. And the patients who are having poor drugs in particular, but also who are what we call maintaining the pressure on the clone, which is trying not to have too many breaks and cheek moments so that any stray cells start to grow. And how important that was and how this has resulted in some very impressive increases in the kind of the response rates and survivals for patients with fibres. So what we see for the future is a diagnostic test upfront, new treatment, probably four drug regimens, plus or minus a T cell engaging therapy assessment of your response, get 100 percent of people to no detectable disease and then monitor their disease over time. And if you see evidence of the disease coming back, start in treatment long before they get clinical signs or symptoms of disease. So functionally, people are cured and functionally, they live a normal and full duration of life.