DNA repair, IFN-α response, fatty acid metabolism, peroxisome, and bile acid metabolism, etc. were significantly strengthened in NAFLD, while KRAS signaling upregulation, IL2-STAT5 signaling, angiogenesis, P53 pathway, and inflammatory response, etc. were significantly weakened in NAFLD (Fig. 8A). This evidence concerns the gene KRAS and metabolic dysfunction-associated steatotic liver disease.