Overexpression of ALCAT1 in primary hepatocytes leads to several features of NAFLD including steatosis, impaired autophagy, and mitochondrial dysfunction, whereas deletion of ALCAT1 restores mitophagy and reduces steatosis, reinforcing a link between mitophagy and NAFLD46, as we observed here. The gene discussed is LCLAT1; the disease is metabolic dysfunction-associated steatotic liver disease.