All of these menin inhibitors that effectively disrupt the menin-MLL interaction lead to decreased expression of KMT2A target genes, inducing differentiation and apoptosis of leukemic cells, and have dramatic activity in early clinical trials in patients with heavily pretreated relapsed or refractory KMT2A-rearranged or NPM1-mutated AML [44, 45]. This evidence concerns the gene KMT2A and acute myeloid leukemia.