SMAD2 and aneurysm: Nonetheless, a well-documented molecular feature of syndromic aneurysm tissue from humans and genetically engineered mice is evidence for paradoxical, hyperactivated canonical TGFβ signaling in smooth muscle cells, as determined by immunostaining for phosphorylated SMAD2/3 (pSMAD2/3) (Gomez et al., 2009; Habashi et al., 2006; Holm et al., 2011; Lindsay et al., 2012; Loeys et al., 2005).