 Actually, actually, there weren't too many things about AL amyloidosis. We do have older things that were published, like the final results of the vital study with an antibody to dissolve the amyloid, which didn't work at the end, but at least we can see now the results. And there was a nice presentation this morning regarding the tourmaline study, which is a study comparing an oral proteasome inhibitor, which is called exasome, as compared with standard of care therapy for relapsing patients with AL amyloidosis. This clinical trial was actually, I tried, it was designed a few years ago, and the company should be commended because it's the first clinical trial done in AL amyloidosis, which is randomized, meaning that there were two groups of patients and they were comparing two kinds of treatments for this group of patients. One group of patients got the study drug, which is exasome, which is the oral proteasome inhibitor, like the bortezomib only given orally, and it was compared to the standard of care at the time, which was either Revlimidindexamethasone or Melphalanindexamethasone, also other possibilities like cyclophosphamide or Ptolydomide. These were the available options six or seven years ago when the trial was designed. So the results showed that for the primary objective of the trial, which is to compare the response rate, the hematologic response rate, results were pretty much similar when you compare the exasome with the other medications. However, so exasome at least was as good as the standard of care, the interesting thing is that with exasome, the results were a little bit better in terms of the depth of the response. So the responses were more durable, they were for a more prolonged time, and also the depth of the response, not just the hematologic response, but as far as we can get with lowering the free light chain levels, it was better with exasome. Even this translated into a better organ response, meaning that patients that had either cardiac or renal involvement got better a long time when they were treated with this medication. So patients who do not achieve rheumatologic response, we do know that the light chains themselves are toxic to the organs, meaning in a way that when the response is not good enough, the light chains don't go as low as we'd like, and this becomes toxic to the organs themselves apart from being within the organs. And so our goal in treatment is to lower the light chains as much as possible. So if we do not do that, that means that we don't get a hematologic response. And this is correlating to worse outcomes of the patients, meaning that they either survive less or even their organs are less amnable to get better a long time. And so when the patients have a better hematologic response, kind of very good hematologic response or even completely hematologic response, this is parallel to better organ response and survival most probably. Well that is a good question because the trial was designed six or seven years ago. And six or seven years ago we had not too many options and more options come to the myeloma field, so there's more options come to the amyloid field. So yes, in a way, X-asomib will probably become a very good medication to use in alamyloidosis, but nowadays we have other medications apart from that, like dartumab and other novel agents. So we might be using a combination or new combinations apart from using X-asomib because of the good results we get with it. So preclinical identity too many studies in this ash, clinical studies are mostly looking at combination therapy, more initial therapies that are coming into consideration in alamyloidosis like as I said dartumab, which are reports of it being very effective in alamyloidosis patients and not just very effective but very prolonged remissions that are continuing with using this medication. Well interestingly there is a Chinese abstract talking about the addition of an antibiotic which is called doxycycline to the treatment. This is being a paradigm that we have lately during the last few years started to use for cardiac patients and we don't really know if it's good enough or not or if it's really doing what it's supposed to be doing to stabilize the amyloid in the fibrils in any way and this abstract seems interesting because it may give an answer whether it's a good medication or not to be added.