The genes included encoding epigenetic modifiers, transcription factors and mediators of cytokine signaling (Tet2, Runx1, Dnmt3, Ezh2, Nf1, Smc3, p53 and Asxl1), thus mimicking the genetic combinations observed in patients with AML and leading to myeloid clonal expansion and transformation to acute leukemia. This evidence concerns the gene RUNX1 and acute myeloid leukemia.