In RA, excessive infiltration of circulating leukocytes into the inflamed joint induces synovial tissue macrophages and fibroblasts to produce inflammatory and proangiogenic factors, such as TNF-α, IL-1β, IL-6, IL-17, and TGF-β that trigger neoangiogenesis (95, 106, 107). This evidence concerns the gene TNF and rheumatoid arthritis.