As this patient was pretreated with a DNMT3A inhibitor (azacitidine) and as gilteritinib is effective for patients with relapsed or refractory AML with FLT3 genetic mutations, we presumed that gilteritinib is potent enough to remodel chromatin landscape from an abnormal into a normal state. The gene discussed is FLT3; the disease is acute myeloid leukemia.