Rheumatoid arthritis (RA) is a multifactorial polygenic disease that is both common (about 0.5% among adults) and severe. It is a systemic inflammatory and autoimmune disease where clinical manifestations predominate in the joints. Although the trigger is unknown, the cascade of immunological and inflammatory responses has been documented in detail [1]. These responses lead to inflammatory synovitis with angiogenesis and infiltration by mononuclear and polynuclear cells within the joint. Synovial inflammation also heralds irreversible bone and joint destruction. Studies highlighting the key role of proinflammatory cytokines in RA have allowed the development of treatment targeting those