Proinflammatory cytokines, such as interleukin- (IL-) 1, IL-6, and tumor necrosis factor-alpha (TNF-α), produced within locally affected joints in RA may promote both traditional [e.g., dyslipidemia and insulin resistance (IR)] and nontraditional (e.g., oxidative stress) systemic cardiovascular risk factors [2]. This evidence concerns the gene TNF and rheumatoid arthritis.