Defective control of the systemic inflammatory response and the development of autoimmunity, often emerging long before the clinical onset of the disease, result in the synovial infiltration and activation of immune and stromal cells that lead to the production of high levels of inflammatory mediators such as pro-inflammatory interleukins (IL-1, Tumor Necrosis Factor-TNF-α, IL-6) or matrix metalloproteinases (MMP) (1). The gene discussed is TNF; the disease is Autoimmunity.