The potential role of IFNs in NAFLD has been demonstrated by an increased expression of stimulator of IFN genes (STING) in high-fat diet (HFD)-induced NAFLD mouse model and free fatty acid-induced NAFLD in the human fetal hepatocytes cell culture, whereas knocking down either STING or IRF3 reduced the lipid accumulation, hepatic inflammation, and apoptosis in liver of mice [84]. The gene discussed is IRF3; the disease is metabolic dysfunction-associated steatotic liver disease.