Consistent with our results, the detrimental effects of increased elastolysis, oxidative stress, and impaired elastin cross-linking in promoting aortic dilation have also been previously reported in the Ang II-infused, the elastase-perfused, the fibrillin-1 knock-out/Marfan syndrome, and the LOX knock-out murine models.11–13,29,37,44–47. The gene discussed is FBN1; the disease is Marfan syndrome.