Beside the role of hepatic SREBP2 in the pathophysiology of NAFLD/NASH, our studies in transgenic mouse model of intestine-specific overactivation of SREBP2, demonstrated hepatic steatosis, and increased susceptibility of the animals to severe liver damage and profound inflammation and fibrosis in response to a high fat/high cholesterol diet (41). This evidence concerns the gene SREBF2 and metabolic dysfunction-associated steatotic liver disease.