Consistent with the amelioration of the steatotic phenotype, Acod1 loss counteracted the HFD-induced hepatic accumulation of perilipins (PLIN2, PLIN3, PLIN4), which sequester lipids by protecting lipid droplets from lipase action, enzymes responsible for peroxisomal fatty acid β-oxidation (ACOX1, HSD17B4, SCP2, CRAT, ACOT2, ACOT4, DECR2), known to promote HFD-induced liver steatosis by inhibiting hepatic lipophagy [22], as well as CD36 which promotes fatty liver development by facilitating free fatty acid (FFAs) uptake in hepatocytes [23, 24] (Fig. 2F). Here, CD36 is linked to fatty liver disease.