Similar to PPARα, treatment of platelets with synthetic ligands of PPARβ/δ have been shown to cause an increase in intracellular cAMP levels and PKCα has been identified as a potential binding partner of the receptor indicating a plausible mechanism by which PPARβ/δ regulates platelet reactivity (Figure 2)35 PPARβ/δ ligands have been shown to decrease plaque formation and attenuate the progression of atherosclerosis.59 This evidence concerns the gene PPARD and atherosclerosis.