Patients with therapy-related AML were more likely to be associated with TP53 and ABC family gene mutations and less likely to have DNMT3A and NPM1. In our study, none of the patients harbored TP53 or ABC family gene mutations at relapse, and two relapsed with DNMT3A. The absence of common cytogenetic and molecular abnormalities seen in therapy-induced leukemia suggests other mechanisms for late relapse. Here, NPM1 is linked to acute myeloid leukemia.