The inhibition of CXCL8 reduces angiogenesis in RA, and the release of CXCL12 from FLS could inhibit the pro-angiogenic activity of other chemokines and VEFG by binding to CXCR4 or CXCR7 (188, 189). The gene discussed is CXCL8; the disease is rheumatoid arthritis.