Certain reports revealed that the CXCR4 antagonist plerixafor (AMD 3100) selectively reduced the proliferation of FLT3-ITD AML blasts and increased the sensitivity of FLT3-mutated leukemic cells to the apoptogenic effects of FLT3 inhibitors [93,94]; therefore, the activation of the CXCL12/CXCR4 axis may also induce resistance to FLT3 inhibitors in AML cells. The gene discussed is CXCR4; the disease is acute myeloid leukemia.