The pathogenesis of RA is complicated; lymphocytes, plasma cells, and macrophages infiltrate the synovium form and cause synovial hyperplasia and the expression of proinflammatory cytokines such as IL-1β, IL-6, IL-17, and TNF-a, which have been reported to play a role in the pathogenesis of RA [3, 4]. Here, IL1B is linked to rheumatoid arthritis.