FLT3 and acute myeloid leukemia: On the basis of our work here and our previous work (24), GSK-3β  activation appears to be an effective strategy for optimizing response to FLT3 inhibitors, through posttranslational downregulation of c-Myc, Mcl-1, and Pim-1, key proteins driving proliferation and resistance to apoptosis in AML cells with FLT3-ITD.