KMT2A and acute myeloid leukemia: Interestingly, while the interaction of MEN1 with MLL1 is not essential for normal hematopoiesis (114), genetic disruption of the MEN1-MLL fusion protein interaction abrogates the oncogenic properties of MLL fusion proteins and blocks the development of AML in vivo (113), highlighting this interaction as an attractive therapeutic target to develop targeted drugs for MLL leukemia patients.