We have defined a molecular signature for identifying responders to azacytidine therapy, characterized by the presence of mutations in DNMT3A, TET2, EZH2, or U2AF1. In this context, mutations in TET2 have previously been associated with responses to HMAs in MDS, or in AML with 20–30% blasts [7,21]. Here, DNMT3A is linked to acute myeloid leukemia.