Autoreactive T cells, B cells (action as professional antigen-presenting cells, antibody-dependent cell-mediated cytotoxicity, and proinflammatory cytokine-producing cells), and inflammatory cytokines such as TNF-α and IL-6 play a pivotal role in the pathological processes of RA through the accumulation of inflammatory cells, production of matrix metalloproteinase, and induction and/or activation of osteoclasts, leading to the destruction of cartilage and bone [27–29]. This evidence concerns the gene TNF and rheumatoid arthritis.