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The prevalence of nonalcoholic steatohepatitis (NASH) — the more severe form of nonalcoholic fatty liver disease (NAFLD) — continues to increase and there are currently no available therapeutics. A major hurdle in the development of drugs for NASH is a lack of reliable preclinical models. Recently, perturbation in amino acid metabolism was implicated in NASH, with impaired glycine metabolism identified as a causative factor and therapeutic target. Subsequently, a glycine-based tripeptide, DT-109 (Gly-Gly-Leu), was reported to lower steatohepatitis and hepatic fibrosis via induction of fatty acid (FA) degradation and antioxidant defence through de novo glutathione (GSH) biosynthesis. Now, Qu et al. have developed a non-human primate model of NASH, which histologically and transcriptionally mimics the human disease. When the primates were treated orally with DT-109 for 5 months, diet-induced hepatic steatosis was reversed and hepatic inflammation and fibrosis was blocked, without toxicity. A multiomics approach demonstrated these beneficial effects to be mediated not only by stimulating hepatic FA degradation and GSH formation, but also by modulating the gut microbiota to enhance Faecalibacterium, which inhibits the production of the secondary bile acid, lithocholic acid (LCA). Circulating LCA was significantly increased in patients with NAFLD compared to healthy controls.