For the pathogenesis of RA, proinflammatory cytokines – especially tumor necrosis factor alpha (TNFα) – were shown to play one of the most important roles in RA pathogenesis by stimulation of matrix metalloproteinase and proteolytic enzyme release from synoviocytes leading to local cartilage degradation and demineralization of bone in affected joints [2]. The gene discussed is TNF; the disease is rheumatoid arthritis.