INS and metabolic dysfunction-associated steatotic liver disease: In light of the above-mentioned role of hepatocyte CB1R, a recent study by Wang and colleagues raised concerns about the reproducibility of the effects seen in hepatocyte-specific CB1R−/− mice, by demonstrating that deletion of CB1R in hepatocytes did not alter de novo lipogenesis, insulin resistance, or the development of NAFLD in response to an HFD [80].