ER stress in NAFLD promotes lipogenesis, impairs lipid metabolism, and disrupts insulin signaling pathways, contributing to the development of hepatic steatosis (accumulation of fat in the liver) and the progression of NAFLD to more severe forms, such as non-alcoholic steatohepatitis (NASH) and fibrosis [39–41]. Here, INS is linked to metabolic dysfunction-associated steatotic liver disease.