In the evolution of atherosclerosis, SMC changes their phenotype expression; in healthy vessels, SMCs exhibit α-smooth muscle actin (αSMA), while upon injury or atherosclerosis, these switch to a synthetic phenotype mediated via platelet-derived growth factor-BB and Klf4, which is inhibited by miRNA143/145 and TGF-β (108). This evidence concerns the gene KLF4 and atherosclerosis.