Rheumatoid arthritis (RA) is a systemic autoimmune disease characterized by chronic synovitis of the joints, in which cytokines such as tumor necrosis factors (TNFs) and interleukins (ILs) contribute to the pathogenesis, causing excessive bone resorption and chondral degradation, and resulting in articular deformities [1]. This evidence concerns the gene TNF and rheumatoid arthritis.