TLRs activation hasbeen linked to the pathogenesis of rheumatoid arthritis, and both TLR-2 andTLR-4 are potentially critical receptors in the initiation and perpetuation ofthe inflammatory cycle in arthritis [3].It has been also demonstrated that endogenousTLR4 ligands (e.g., heat shock proteins and extra domain A fibronectin) arehighly expressed in the joints of patients with RA [4–6].Toll-like receptors are present on tissuesynoviocytes but also on peripheral blood monocytes which are recruited to thesite of inflammation and areinvolved in the pathogenesisof synovial inflammation [7–10]. The gene discussed is TLR2; the disease is rheumatoid arthritis.