We recently demonstrated that the aberrant expression of MEIS1, PBX3, and several HOX transcription factor genes in the NPM1 mutated AML depend on the Menin-KMT2A (wildtype) protein interaction, represent a therapeutic opportunity and early Menin inhibitors had activity against preclinical models of this leukemia subtype [39]. This evidence concerns the gene NPM1 and acute myeloid leukemia.