Recent research has underscored the pivotal roles of these ER stress and UPR sensors in the development of hepatic steatosis.[70] For instance, activated IRE1α enhances the transcription of serine palmitoyl transferase genes via XBP1s, facilitating the biosynthesis of ceramides and the release of extracellular vehicles from hepatocytes.[71] In diet-induced NASH models, these EVs attract macrophages to the liver, exacerbating inflammation and furthering liver injury associated with diet-induced steatohepatitis. The gene discussed is ERN1; the disease is fatty liver disease.