Prevention of oxidative damage and apoptosis in patient-derived aortic VSMCs or aortic dilatation in the zebrafish model by antioxidants, together with proven efficacies of α-tocopherol or a mitochondrial ROS scavenger in preventing AAA formation in mouse models31, raises the possibility of antioxidant therapy to prevent aortopathy in patients with SECISBP2 mutations. Here, SECISBP2 is linked to triple-A syndrome.