Genetic models of NAFLD include AOX null mice [6,7], MAT1A null mice [8], liver-specific NRF1 knockouts [9], liver-specific PTEN knockouts [10] and leptin-deficient obese mice [11,12], which develop NAFLD due to a disruption in the antioxidant mechanism, fatty acid metabolism or triglyceride synthesis/secretion. Here, ACOX1 is linked to metabolic dysfunction-associated steatotic liver disease.