Syndromic aneurysms (Marfan syndrome and other connective tissue diseasesincluding Loeys-Dietz syndrome, Ehlers-Danlos syndrome, and familial TAAD) havebeen proven to have overlapping clinical features and mutated TGF-βgenes[23,24] while familial non-syndromicpatients are associated with mutations in MYH11, transforming growth factorbeta-receptor 1 (TGFβR1), Transforming growth factor beta-receptor 2(TGFβR2), myosin light chain kinase (MYLK), and ACTA2 genes in spite ofincomplete penetrance and/or locus heterogeneity[24]. This evidence concerns the gene TGFBR2 and familial thoracic aortic aneurysm and aortic dissection.