First of all, low efficacy as a result of multiple resistance mechanisms specifically off-target mutations mainly decreased the potency of these inhibitors against FLT3 overexpressing AML cells, and this made these inhibitors potent only when included within combinatorial therapy regimens with other anticancer agents (such as Doxorubicin, Cytarabine, and Anthracycline). The gene discussed is FLT3; the disease is acute myeloid leukemia.