KMT2A and leukemia: The heterozygous FLT3-ITD mutation does, however, cooperate with other molecular lesions in mouse models to generate both myeloid and lymphoid leukemia, such as MLL-AF9 (78), mutant C/EBPα (79), NUP98–HOXD13D (NHD13) fusion (80), and mutant nucleophosmin (NPMc+) (81), in agreement with accumulating evidence that leukemogenesis is a process that requires multiple genetic or epigenetic “hits.” Interestingly, a mouse model of homozygous FLT3-ITD mirrored the increased disease severity of CN-LOH seen in human malignancy with some homozygous mice developing spontaneous leukemia (77).