I think we had a great session today here in Marseille. It’s kind of been exciting to hear how everybody’s understanding more about how the microenvironment inflammation and our immune system play a role in the development of and progression of MDS. Whether it’s through acquired somatic mutations like in UBA1 that have contributed to this newly formed entity of VEXAS, or if it’s the expansion of clonal progenitors and clonal hematopoiesis in the setting of inflammation and aging...
I think we had a great session today here in Marseille. It’s kind of been exciting to hear how everybody’s understanding more about how the microenvironment inflammation and our immune system play a role in the development of and progression of MDS. Whether it’s through acquired somatic mutations like in UBA1 that have contributed to this newly formed entity of VEXAS, or if it’s the expansion of clonal progenitors and clonal hematopoiesis in the setting of inflammation and aging. I think that we are understanding that there is a significant role that is played not only in mutated malignant disease and pre-clonal disease as well as kind of the rest of the milieu in which they live. So T-cells and NK cells, macrophages, other cells that interact with MDS cells. So, while we are looking at ways and hoping to see an improvement in how we treat MDS and maybe a new therapy be approved in the coming years, at the same time, I think we understand that MDS is heterogeneous but targeting the immune system and continues to be a modality that we’re looking at.