The hTNFtg model (known as Tg(TNF)197Gkl) possesses an insertion of a 3′-modified human TNF transgene which greatly increases TNFα mRNA stability resulting in systemic overproduction of human TNFα.2 In the TNFΔARE mouse, the 3′ untranslated region (UTR) of the AU-rich element (ARE) in the murine TNFα gene is deleted, resulting in greatly increased TNFα mRNA stability and systemic overexpression.6 As a consequence, inflammation is driven by the overexpression of TNFα in all major tissues resulting in polyarthritis and joint destruction in both models. The gene discussed is TNF; the disease is polyarticular arthritis.