The pathogenesis of RA includes overexpression of proinflammatory cytokines, such as tumor necrosis factor (TNF)-α, interleukin (IL)-6, IL-1β, and matrix metalloproteinase 3, in the synovial fluid, and lymphocyte infiltration in the synovial membrane [4, 5]. This evidence concerns the gene IL6 and rheumatoid arthritis.