As proinflammatory cytokines and metabolic abnormalities associated with systemic inflammation are considered one of principal mechanisms leading to endothelial dysfunction in patients with RA [2, 11], we looked for the relationship between systemic inflammatory markers (ESR, hsCRP, TNF-α, and IL-6) and biochemical measures of endothelial activation (vWf, MCP-1, ADMA, sVCAM-1, sE-selectin, OPG, and PTX3). The gene discussed is CCL2; the disease is endothelial dysfunction.