Moreover, chondrocytes can also express toll-like receptor (TLR)-1, TLR-2, and TLR-4, and activation of TLR-2 by IL-1, TNF-α, peptidoglycans, lipopolysaccharide, or fibronectin fragments increases the production of MMPs, prostaglandin E (PGE), and vascular endothelial growth factor (VEGF) [34], all of which are mediators in inflammation and angiogenesis, the central step in RA pathogenesis [3]. This evidence concerns the gene VEGFA and rheumatoid arthritis.