Despite their opposite action in lipid metabolism, PPAR and LXR enjoy some common features and have anti-atherosclerotic effects. PPAR controls the cholesterol efflux in foam cell macrophages through the LXR-dependent ATP-binding cassette (ABC) pathway and activation of PPAR inhibitors foam cell formation and thereby atherosclerosis [42, 43]. Activation of the LXR upregulates the expression of ABCA1 and ABCG1 and accelerates reverse transport of cholesterol [44]. Here, PPARA is linked to atherosclerosis.