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). The gene discussed is CCR5; the disease is neoplasm.