PPARγ, a ligand-dependent transcription factor that can regulate fatty acid storage and glucose metabolism, plays a vital role in NASH.28,29 Increasing evidence has indicated that PPARγ activation might inhibit the inflammatory responses in the liver of NASH rats.30 There is growing evidence affirmed that PPARγ agonist rosiglitazone could alleviate hepatocyte steatosis through inhibiting the activation of STAT3 pathway.31 However, the long-term use of rosiglitazone might cause adverse reactions such as weight gain, fluid retention, and an increase in the risk of heart disease. The gene discussed is STAT3; the disease is metabolic dysfunction-associated steatohepatitis.