The pathophysiology of RA is characterized by a variety of immune cells with aberrant inflammatory cytokines such as TNF-α, IL-1, IL-6, and IL-17, infiltrating in the synovium of multiple joints, and those inflammatory mediators lead to long-term inflammation and the formation of pannus, which ultimately result in irreversible joint and cartilage destruction and sever disability [2, 3]. Here, TNF is linked to rheumatoid arthritis.