Anticyclic citrullinated peptide antibodies (anti-CCP), IgM rheumatoid factor, circulating immune complexes, proinflammatory cytokines including TNFα and IL-6, Th0/Th1 cells, decreased folate and vitamin B12 productions, and impaired paraoxonase activity, among others, may all be further involved in the development of vascular disease in RA [85–87]. The gene discussed is TNF; the disease is rheumatoid arthritis.