Targeting this system, either by hepatocyte-specific knockout of peroxisomes or by deficiency in ACOX (which catalyzes the initial step in peroxisomal FAO), results in hepatic lipid accumulation and fibrosis, oxidative stress, and inflammation, emphasizing the role of peroximal FAO in NAFLD and NASH [108]. The gene discussed is ACOX1; the disease is metabolic dysfunction-associated steatotic liver disease.