In addition to the direct inhibitory effects on NAFLD and atherosclerosis, PPARδ, AMPK, and PGC-1α activate the catabolic metabolism in cells as a basal mechanism of anti-NAFLD and antiatherosclerosis: PPARδ and AMPK activate oxidative phosphorylation and anti-inflammation, and PGC-1α is involved in mitochondrial biogenesis and increases oxidative phosphorylation [41–43]. Here, PPARGC1A is linked to atherosclerosis.