Rheumatoid arthritis (RA) is a chronic systemic autoimmune disease characterized by a symmetrical inflammation of the synovium, resulting in tenderness and destruction of bone and cartilage in various joints, particularly the smaller joints of the hands and feet. Although the cause of RA is unknown, autoimmunity plays a pivotal role in its chronicity and progression. RA affects approximately 1.0% of the general population, women more often than men, and the inflammatory burden of the disease results in functional disability.[1] Several contributors to RA pathogenesis have been identified in recent years: genetic factors (shared epitope on locus HLA–DRB1, but also PTPN22, STAT4, 6q23 and TRAF1/C5), cigarette smoking, autoantibodies (rheumatoid factor (RF), anti–cyclic citrullinated protein antibodies (ACPA)), infectious agents, as well as nutritional and hormonal factors. [2] Ultimately, an interplay between these endogenous and exogenous factors has been postulated to break immunological tolerance and trigger the immunological response that manifests itself as RA. [3]The immunological activation of RA leads to infiltration of the synovium by an orchestra of immune cells like T and B cells, macrophages, dendritic cells and fibroblast–like synoviocytes, contributing to the proliferation of cell tissue (i.e. pannus formation) and neovascularization.[4] These immunological processes perpetuate systemic inflammatory responses, leading to a chronic, disabling disease which results in the inability to work and an impaired quality of life. [5]