Although the exact mechanisms by which NPM1m contributes to AML still need to be fully understood, in NPM1m AML, the wild-type MEN1-KMT2A complex directly interacts with highly expressed levels of HOXA and MEIS1, paralleling the genetic profile observed in KMT2Ar AL [8,12,34]. This evidence concerns the gene KMT2A and acute myeloid leukemia.