CONCLUSIONS: The improvement of NAFLD by GR may be primarily achieved through its active components (such as ellagic acid and terchebin) via modulation of key targets (such as STAT3) and signaling pathways (such as PI3K/AKT/mTOR), thereby regulating lipid metabolism, alleviating oxidative stress and insulin resistance, and exerting therapeutic effects. The gene discussed is MTOR; the disease is metabolic dysfunction-associated steatotic liver disease.