CXCR4 can be activated in cancer cells through the following mechanisms: (i) hypoxia upregulates the CXCL12–CXCR4 axis [27]; (ii) CXCR4 regulates stem cell pluripotency and cell fate decisions through Wnt/β-catenin, which in turn positively modulates CXCR4 expression [25,28]; (iii) NFκB induces CXCR4 expression and stimulates tumor invasion [29]. Here, CXCL12 is linked to neoplasm.