Three main mechanisms have been described [6]: autoantibody production, viral epitopes, structurally similar to self-ones, can induce the activation of both T- and B-cells through their presentation by APCs, enhanced cytokine-mediated release by T lymphocytes, and vascular damage .In this regard, it is important to point out that RA patients tend to display expansion of a particular subset of T-cells CD4+ lacking the costimulatory molecule CD28, which causes major coronary damage. The gene discussed is CD4; the disease is rheumatoid arthritis.