Studies based on mouse models have highlighted that AML, driven by potent oncogenes, such MLL fusion, may have developed via committed myeloid progenitors (CMP) whereas AML without any major cytogenetic abnormalities may emerge due to a combination of preleukemic initiating events arising in the hematopoietic stem cell (HSC) pool (15). Here, KMT2A is linked to acute myeloid leukemia.