Finally, to functionally validate candidate genes from these derepressed programs as potential mechanistic effectors of the accelerated AML induction following Ezh2 loss in vivo, we generated retroviral constructs for Plag1 and Lin28b. These genes were overexpressed along with MLL-AF9 in WT Ezh2+/+ HSPCs. The gene discussed is KMT2A; the disease is acute myeloid leukemia.