In combination with Tet2MT, oncogenic kinase mutations such as Jak2V617F, Flt3ITD, and KitD816V promote NPM and AML development by inducing the uncontrolled proliferation of Tet2MT myeloid progenitors by stimulating Akt-mTor and Jak-Stat5 signaling. This evidence concerns the gene STAT5A and acute myeloid leukemia.