Kinase inhibition—Internal tandem duplication mutations resulting in constitutive activation of the FMS-like tyrosine kinase receptor 3 (FLT3-ITD) are present in approximately 20%–30% of cases of AML, represent a high-risk feature in normal karyotype AML, and are associated with a high risk of relapse following alloHSCT [103]. Here, FLT3 is linked to acute myeloid leukemia.