Hyperproduction of proinflammatory cytokines (interleukins (IL)-1, 6, 17, tumor necrosis factor α— TNF-α) and growth factors in RA promotes the liberation of proteolytic enzymes (matrix metalloproteinases—MMPs) by synovial cells causing the destruction of connective tissue of the joint [8] and stimulates an increased production of receptor activator of nuclear factor NF-κB ligand (RANKL) [9, 10]. The gene discussed is TNF; the disease is rheumatoid arthritis.