In contrast to endothelial cells, deleting Ceacam1 in hepatocytes caused hyperinsulinemia-driven systemic insulin resistance and visceral obesity associated with features of non-alcoholic fatty liver disease and atherosclerosis when mice were backcrossed on the Ldlr null background and fed an atherogenic diet for 3 months [21]. This evidence concerns the gene LDLR and metabolic dysfunction-associated steatotic liver disease.