Other metabolic causes of hepatic steatosis, include long-chain FAs (LCFAs) β-oxidation within peroxisomes and ω-oxidation in ER, both overexpressed in NASH; and defects in the mitochondrial trifunctional protein (MTP), which catalyzes β-oxidation of LCFAs, promoted hepatic insulin resistance and steatosis development, including an increase in antioxidant defenses and cytochrome P-450 to counteract ROS production [156,241]. This evidence concerns the gene INS and steatosis.