To examine the clinical relevancy of SMAD3 deficiency in the pathogenesis of non-syndromic form of human AAA, we re-examined SMAD3 mRNA expression in our previously published microarray analyses of human aneurysmal and non-aneurysmal abdominal aorta tissue31: SMAD3 mRNA expression was significantly reduced in AAA tissue (Fig. 5A). The gene discussed is SMAD3; the disease is triple-A syndrome.