In hepatocyte-specific AEG-1 transgenic mice (Alb/AEG-1), inhibition of PPARα and FAO leads to spontaneous NASH development—a condition that is reversed in hepatocyte-specific AEG-1 knockout (AEG-1ΔHEP) mice, suggesting a protective role against diet-induced NASH in the absence of AEG-1 [176]. Here, PPARA is linked to metabolic dysfunction-associated steatohepatitis.