Toll-like receptor-4 (TLR-4) also contributes to progression of RA via promoting inflammation-driven angiogenesis through certain cytokines such as tumor necrosis factor–alpha (TNF-α), interleukin-6 (IL-6), and interleukin-1 beta (IL-1β) [12, 13]. This evidence concerns the gene IL1B and rheumatoid arthritis.