TGFBR2 and triple-A syndrome: Mice with deficiencies in Smad3, Smad4, and TGFB2 develop aneurysms, and TGFBR2 deletion causes TAAD in postnatal mice [24,49], while Baas et al. [87] found that variants in TGFBR1 and TGFBR2 were associated with increased AAA risk.