In AML harboring rearrangements of mixed lineage leukemia (MLL), now also know as KMT2A, menin directly interacts with the KMT2A fusion protein to form a transcriptional complex which further drives aberrant gene expression (HOX, MEIS1, and PBX3) that blocks normal myeloid differentiation and promotes leukemic transformation [60,61]. This evidence concerns the gene MEN1 and acute myeloid leukemia.