Similar to our observations, using a mouse model with specific hepatic-HIF-1α deficiency, Mesarwi et al. revealed that although HIF-1α was required for the pathogenesis of liver fibrosis, while it did not have a role in the hepatic TG accumulation [19], and it might even play a protective role in non-alcoholic fatty liver disease by reducing lipotoxicity [20]. This evidence concerns the gene HIF1A and metabolic dysfunction-associated steatotic liver disease.