Intravenous administration of anti-CD3–specific antibodies effectively suppresses effector T cell immune responses and reduces atherosclerosis in mice by inducing TGF-β–producing CD4+CD25+ LAP+ Tregs, which in turn inhibit experimental autoimmunity in a TGF-β–dependent manner (95, 96). The gene discussed is TGFB1; the disease is atherosclerosis.