Genetic studies have revealed a large number of aberrations in AML patients.1, 2 Prognostic gene‐gene interactions have also showed mutations in NRAS, DNMT3A, NPM1, DNMT3A, and IDH2R140.1, 2 The mutated genes/proteins lead to the dysfunction of multiple kinases in AML, which may explain the failure of single kinase inhibitor administration: the dysfunctional kinase pathways compensate each other when pharmaceutical inhibition occurs. Here, DNMT3A is linked to acute myeloid leukemia.