Although these inhibitors have demonstrated promising anti-cancer activity in in vitro and in vivo preclinical models, clinically positive responses in AML patients receiving single-agent FLT3 inhibitors are limited due to the transient reduction of peripheral blasts but not bone marrow blasts or the occurrence of inhibitor-resistant FLT3 mutations in patients [17], [18], [19], [20]. Here, FLT3 is linked to cancer.