Additionally, a previous study shows that the EZH2 "loss-of-function" mutation contributes to formation of the leukemic stem cell by mediating self-renewal of myeloid progenitors [9], indicating that the loss of EZH2 silencing on SEMA3A contributes to leukemogenesis in t-AML. This evidence concerns the gene SEMA3A and acute myeloid leukemia.