FLT3 and acute myeloid leukemia: Interestingly, knockout of this receptor has little effect in hematopoiesis, other than defective repopulation capacities of BM cells upon transplantation.135 This means that active FLT3 signaling is not an absolute requirement for normal blood maintenance, but when it is conversely overactivated in malignant hematopoiesis, by mutations to the FLT3 gene or overexpression, it is frequently a considerable aggressor for AML cell proliferation and survival.