The inflammatory cytokine TNFα plays a crucial role in inflammatory and infectious diseases, from rheumatoid arthritis to septic shock.1 The anti-TNFα therapy has been limited to the treatment of certain inflammatory diseases such as rheumatic arthritis, due to the side effects caused by inevitably abrogating TNFα-mediated beneficial inflammatory response in the host defense against pathogens.2–4 Furthermore, the molecular mechanism underlying TNFα cytotoxicity in disease is obscure, hindering the development of more efficient anti-TNFα-based therapies. The gene discussed is TNF; the disease is rheumatoid arthritis.