Specifically, proinflammatory cytokines such as interleukin-6 (IL-6), IL-17 (Schlegel et al. [2013]) and tumor necrosis factor alpha (TNF-α) play a key role in RA pathogenesis, including the activation of synovial fibroblasts, osteoclasts, and inflammatory mononuclear cells, which results in irreversible damage to the soft tissues and bones (Olsen and Stein [2004]). Here, TNF is linked to rheumatoid arthritis.