The study highlights application of antigen-specific immunomodulation in which Treg-mediated suppression of atherosclerosis requires TLR4/MyD88 signaling and this immunomodulation permits selective inactivation of auto-reactive T cells without interfering with normal immune function [46] as our results have shown the similar profiles of autoantigen ApoB and HSP60 at the lesion sites in both control and sampling animals. The gene discussed is TLR4; the disease is atherosclerosis.