Notably, our findings also highlight different age-related mechanisms driving HCC in the absence of caspase-2 and clear distinctions in the different models used to analyze hepatosteatosis, with MASH models driven by a high-fat or high-fructose diet that trigger a chronic ER stress–related response, dysregulated hepatic lipid metabolism, fat accumulation, inflammation, and fibrosis (29, 47). This evidence concerns the gene CASP2 and hepatocellular carcinoma.