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]. The gene discussed is INS; the disease is metabolic dysfunction-associated steatohepatitis.