We highlighted the theory of tolerance breakdown by the activation of autoimmune lymphocytes via auto-antigens, which was different from genetic mutation-induced autoimmune liver disease in dnTGFβRII mice, IL-2Rα−/− mice and IL-2Rα−/−p40−/− mice, and also differed from xenobiotic- or infection-induced autoimmune liver disease in 2-OA-BSA-immunized mice22, N. aromaticivorans-infected mice23, and E. coli-infected mice24. Here, IL2RA is linked to autoimmune hepatitis.