FLT3 and neoplasm: Given the cross-talk between CXCR4 expression and FLT3-ITD, supported by the activation of CXCR4 signaling by FLT3-ITD and higher CXCR4 expression in FLT3-ITD-AML [14,16], our group first demonstrated the proof of concept that a small molecular CXCR4 inhibitor, AMD3465, could enhance anti-leukemia effects of a multi-kinase inhibitor, sorafenib, in a Ba/F3-ITD murine tumor model [9].