Notably, because RA is a systemic autoimmune disease characterized by chronic inflammation of multiple joints and proinflammatory cytokines such as tumour necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, or IL-17 may be reconsidered as the etiology for RA and further leads to the development of targeted therapies [3, 9–11]. The gene discussed is TNF; the disease is rheumatoid arthritis.