However, when used in combination with other common AML lesions, such as KMT2A-PTD, Npm1c mutation, Dnmt3a deletion, and RUNX1-RUNX1T1, expression of Flt3-ITD is capable of producing AML, though with relatively long latency (46, 93–95). This evidence concerns the gene KMT2A and acute myeloid leukemia.