In order to determine when relative rates of mitophagy decline during the pathogenesis of NAFLD, as well as how the loss of PARKIN-mitophagy contributes to the early and late features of NAFLD, we performed time course studies in mito-Keima and LKO mice using a well-established dietary model that induces the full spectrum of NAFLD pathology, specifically steatosis, inflammation and fibrosis25. The gene discussed is PRKN; the disease is metabolic dysfunction-associated steatotic liver disease.