DNMT3A and acute myeloid leukemia: Mutational inactivation of these factors is recurrently observed in patients with MDS and AML resulting in enhanced HSC self-renewal and a decline in the output of differentiated progeny, thus predisposing to leukemic transformation in mice.151 Inactivation of Tet2 or Dnmt3a in HSC resulted in increased myeloid and decreased erythroid gene expression signature resulting in aberrant accumulation of erythroid progenitors in mice.