The close relationship between the gut and liver in regulating embryological, anatomical, and physiological processes suggests an important role for the gut–liver axis in the pathogenesis of liver diseases, including nonalcoholic fatty liver disease (NAFLD), which is the third leading cause of hepatocellular carcinoma (HCC) worldwide.15,16 Evidence from clinical and preclinical studies suggests that dysbiosis in intestinal microbiota, and consequently, the gut–liver axis may directly and/or indirectly modulate response to RT by remodeling the TME in HCC patients via the cGAS–STING–IFN-I axis. This evidence concerns the gene CGAS and metabolic dysfunction-associated steatotic liver disease.