Oral tolerance induction to oxidized LDL [98] or heat shock protein 60 [99] reduced the development of atherosclerosis in Ldlr−/− mice, in association with increased proportion of CD4+CD25+Foxp3+ Tregs in several lymphoid organs and promoted the production of TGF-β or IL-10 in mesenteric lymph nodes upon each antigen stimulation, respectively. The gene discussed is TGFB1; the disease is atherosclerosis.