Atherosclerosis and RA share many common inflammatory mediators, and the mechanisms leading to synovial inflammation are similar to those found in unstable atherosclerotic plaque; levels of inflammatory molecules, such as CRP, fibrinogen and cytokines, including interleukins (IL-s), may be altered in RA and promote proatherogenic activation and endothelial dysfunction, but also associate with other CV risk factors, such as changes in lipid levels, insulin resistance and oxidative stress that further contribute to vascular damage [2–4]. The gene discussed is CRP; the disease is rheumatoid arthritis.