Systemic inflammation that occurs in RA patients involves various pro inflammatory mediators, especially Tumor Necrosis Factor-α (TNF-α) [3] The role of TNF-α against endothelial dysfunction is evidenced by an experimental study conducted by Goodwin et al. (2007) on endothelial aortic cell cultures, where TNF-α lowered nitric oxide (NO) production by endothelial cells [6]. The gene discussed is TNF; the disease is rheumatoid arthritis.