In RA models, an anti-C5 monoclonal antibody fused to a peptide that allows homing to inflamed synovium by binding to the synovial microvascular endothelium in inflamed knee joints prevented synovial inflammation and localized production of IL-6 and TNF-α, as well as C9 deposition, but did not inhibit circulating levels of C5 [240]. The gene discussed is C5; the disease is rheumatoid arthritis.