Given that SOD2 plays a key role in modulating oxidative stress to protect against mitochondrial damage 20,21 and several studies suggest a relative deficiency in established AAA 15, 18, 22, we posit that SOD2 overexpression in aortic aneurysms may correct the mitochondrial dysfunction, forestalling the oxidative damage that contributes to aneurysmal expansion and rupture. This evidence concerns the gene SOD2 and triple-A syndrome.