While proteins regulating lipid biogenesis were overexpressed in NASH HCCs, examples responsible for lipid catabolism, including molecules downstream of peroxisomal proliferating receptor γ (PPARγ) and peroxisome proliferating receptor α (PPARα), as well as other mitochondrial and peroxisomal proteins involved in process of oxidation of fatty acids, such as enoyl-CoA hydratase, mitochondrial (ECHS1), 3-ketoacyl-CoA thiolase, mitochondrial (ACAA2) and fatty acid binding protein 2 (FABP1), were reduced (Table 1). Here, ACAA2 is linked to metabolic dysfunction-associated steatohepatitis.