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GSH-deficient mouse models have been developed by targeting GCL, the rate-limiting enzyme of GSH biosynthesis Liver-specific Gclc knockout mice have 95% depletion of hepatic GSH and develop spontaneous steatohepatitis Universal Gclm deleted mice have 15% of normal hepatic GSH and are protected from liver injuries induced by hepatic insults Animal studies indicate a potential role of hepatic GSH in fine-tuning metabolic and stress responses to liver injuries Acknowledgments This work was supported in part by the National Institutes of Health Grant AA022057 and the NIEHS Center for Environmental Genetics Grant P30 ES06096