The decrease of RIP3 reduces the death of hematopoietic cells, which is related to the occurrence of AML.296 Another study reported that the genetic defect of RIP3 transformed flt3-itd and runxeto-driven mouse bone marrow proliferation into AML by increasing the accumulation of leukemia-initiating cells.297 Therefore, the role of RIP3 in the pathogenesis of AML may be determined by the cellular environment. The gene discussed is FLT3; the disease is acute myeloid leukemia.