Studies showed that DNMT3A mutations induced anthracycline resistance in AML by impairing nucleosome remodeling,160 and evaded chemotherapy and infiltrated the central nervous system in a patient with AML.161DNMT3AR882H-dependent AML cells were sensitive to hypomethylating agents, such as azacytidine (AZA)162 and decitabine.163 In addition, DOT1L could be a therapeutic target,164 and resistin may serve as an ancillary drug for AML patients with DNMT3A mutation.165. Here, DOT1L is linked to acute myeloid leukemia.