Rheumatoid arthritis (RA) is a systemic autoimmune disorder primarily characterized by chronic inflammation of the joints, which progressively leads to bone destruction and joint deformities, resulting in multiple articular disabilities.1 A key factor in RA pathogenesis is the activation of inflammatory macrophages, which secrete a range of pro-inflammatory cytokines, such as tumor necrosis factor-alpha (TNF-α). The gene discussed is TNF; the disease is rheumatoid arthritis.