Long-standing inflammation, as observed in RA, induces the release of proinflammatory mediators such as glucocorticoids; lipopolysaccharides (LPSs); and cytokines, including interleukin-6 (IL-6), interleukin-1β (IL1β), and tumor necrosis factor-α (TNF-α) [15]. This evidence concerns the gene TNF and rheumatoid arthritis.