Anti-IL-1 and TNF-α therapies in animal arthritis models and anti-TNF-α in humans with RA have been shown to significantly reduce arthritis incidence, inflammation and joint destruction [1,6-8], suggesting that the mediating pathways of joint damage are, at least in part, mediated by IL-1 and/or TNF-α. This evidence concerns the gene TNF and rheumatoid arthritis.