Our data were consistent with previous studies in that all seven individuals with mutations in TGFB2, TGFB3 or SMAD2 had relatively mild aortic events, except that patient AD985, who had the risk factors of extreme hypertension and an intronic mutation predicted to affect normal splicing, suffered an aortic dissection at 32 years of age. Here, SMAD2 is linked to dissection.