FLT3 and acute myeloid leukemia: One mechanism by which AML cells can become resistant to FLT3 inhibition is through the development of mutations, either those occurring in FLT3 directly such as the F691L mutation which prevents the binding of Gilteritinib to the FLT3 protein,8 or newly developed activating mutations in downstream targets of FLT3, including MAPK pathway genes such as NRAS or KRAS, which have been detected in 38.9% of relapse patients.9