Since TNFα is crucial in chronic immune responses such as rheumatoid arthritis and psoriasis, it seems likely that the W538S mutation has some protective impact on disease development by abrogating release of proinflammatory soluble TNFα which may be in part influenced by also preventing anti-inflammatory effects of soluble TNFRI. The gene discussed is TNFRSF1A; the disease is rheumatoid arthritis.