Previous studies have shown that SMC to SEM cell transdifferentiation mediated by retinoic acid increases atherosclerosis and plaque vulnerability,15 as does SMC to macrophage transdifferentiation mediated by Klf4.14,17 ER stress in medial SMCs also enhances atherosclerosis.27 We thus examined the role of SMC-Abca1/Abcg1 in transdifferentiation of aortic SMCs, using a similar approach to bladder SMCs. Here, KLF4 is linked to atherosclerosis.