GalN, an amino sugar, was used to inhibit cellular transcription activity to potentiate LPS toxicity, which causes liver cell apoptosis and necrosis and then hepatitis and liver dysfunction.21, 22 Our findings suggest that deletion of Cav‐1 suppresses LPS/GalN‐induced lethality, the inflammatory response and hepatic injury. Here, CAV1 is linked to hepatitis A virus infection.