Thus, we analyzed the pathways related to FA oxidation, finding a decreased expression of both ACOX-1 (a rate-limiting enzyme in peroxisomal fatty acids β-oxidation) and CPT1A (a key enzyme in mitochondrial fatty acids β-oxidation) [12] observed in CDAA+CCl4-treated animals at 1 months and in CDAA mice thereafter, indicates that reduced fatty acid oxidation could be one of the mechanisms of hepatic steatosis (Fig. 3E–F). Here, CPT1A is linked to fatty liver disease.