DNMT3A and acute myeloid leukemia: Complete Dnmt3a loss enhances self-renewal in hematopoietic stem cells (HSCs), impairs differentiation, but is not sufficient to drive leukemogenesis in mice; specific disease progression depends on additional genetic alterations, such as Ras mutations [31, 32] Thus, complete loss of Dnmt3a synergizes with KrasG12D, expediting disease progression and culminating in approximately 30% of mice developing AML [30] (Table 1).