 In this study, researchers found that genetic deletion of the malic enzyme I, Mi-1, gene in hepatocytes was associated with increased susceptibility to liver damage caused by ischemia reperfusion, i-slash-R, suggesting that Mi-1 plays a critical role in preventing liver injury during i-slash-R. They also discovered that Mi-1 is regulated by the phosphatase and tensin homologue, PTN, mediated suppression of the mechanistic target of rapamycin-slash-sterole regulatory element binding protein 1, mTOR-slash-SREP1, signaling pathway, which leads to decreased NADPH production and subsequent furoptosis. Furthermore, they showed that increasing NADPH levels can reduce i-slash-R induced liver injury by blocking Mi-1 expression and furoptosis. These results suggest that Mi-1 could be a potential therapeutic target for i-slash-R-induced liver injury. This article was authored by Xue Xinfeng, Jiawei Shang, Yuli, and others.