Moreover, FLT3-ITD-AML has demonstrated enhanced CXCL12/CXCR4 signaling through upregulation of the cell surface expression of CXCR4 [14,16], which suggests that the CXCL12/CXCR4 axis may influence responsiveness to therapy and confer the poor prognosis of FLT3-ITD-AML [16]. The gene discussed is CXCR4; the disease is acute myeloid leukemia.