Since the decreased pro-survival signaling exclusively through the ERK pathway is a mechanism of sensitization of FLT3-ITD-AML to FLT3 inhibitors through CXCR4 blockade, the combination of potent FLT3 inhibition and MEK inhibition could represent a promising strategy for the treatment of FLT3-ITD-AML, which was supported by previous data demonstrating anti-leukemia activity of a MEK1 and FLT3 dual inhibitor, E6201, in AML cells resistant to FLT3 inhibition [34]. The gene discussed is CXCR4; the disease is acute myeloid leukemia.