Based on previous observations that hypomethylating agents may be particularly active in AML with poor-risk disease features, such as adverse-risk genetics, myelodysplasia-related changes, or specific gene mutations (e.g., TP53) [10–12, 35–38], our hypothesis was that these patients would benefit from incorporation of azacitidine within a regimen of intensive induction chemotherapy. Here, TP53 is linked to Myelodysplasia.