It has been shown that patients with AML harboring mutations in NPM1, IDH1/2, or TET2 (and possibly RUNX1 and STAG2 in the relapsed/refractory setting) respond favorably to azacitidine–venetoclax (or decitabine–venetoclax), independently of the underlying karyotype. This evidence concerns the gene NPM1 and acute myeloid leukemia.