EPCs are recruited into ischemic or hypoxic tumours predominantly in response to chemokines (e.g., CXCL12, CCL2, CCL5) and growth factors (e.g., VEGF, bFGF), which interact with their respective receptors (e.g., CXCR4, CCR2, CCR5, VEGFR2) on the surface of EPCs (De La Puente et al., 2013). This evidence concerns the gene CXCL12 and neoplasm.