Intriguingly, although we know that patients with ACTA2 genetic mutations can develop familial thoracic aortic aneurysms, this finding suggests that redox modifications to the normal α‐SMA protein may potentially promote aneurysm formation.28 ROS can affect multiple additional downstream effectors during AS aneurysm formation, including enhanced (a) MMP activation; (b) SMC apoptosis; and (c) SMC phenotype switching.42, 46 Here, we describe the important relationship between ROS and protease activity, both in vitro and in vivo. Here, ACTA1 is linked to thoracic aortic aneurysm.