In summary, our findings indicated that the liver-specific deficiency of BAP31 enhanced APAP-induced liver toxicity in mice due to the weakening of Nrf2 signaling and the increased oxidative stress, pointing to the protective roles of BAP31 in the pathogenesis of APAP-induced hepatotoxicity, suggesting BAP31 as the potential therapeutic target for liver diseases caused by APAP overdose. This evidence concerns the gene BCAP31 and liver disorder.