Regarding this, it has been described that MIF can be stimulated by the persistent proinflammatory response in RA, and that it can promote the activation of phospholipase A2 (PLA2) and the production of cyclooxygenase-2 (COX-2) and prostaglandin E2 (PGE2) in multiple immune cells that are associated with joint inflammation and the promotion of the production of proinflammatory cytokines that play a crucial role in early and established RA, such as TNF-α, interferon (IFN)-γ, IL-1β, IL-6 [3], and IL-17 [4]. This evidence concerns the gene TNF and rheumatoid arthritis.