TGFB1 and Marfan syndrome: Smooth muscle cell dysfunction (modulation from contractile to the dedifferentiated synthetic phenotype) is known to contribute to aortic aneurysm development in a variety of hereditary aneurysm phenotypes.16, 17, 18 Crosas‐Molist et al19 demonstrated that SMCs in MFS patients actually display increased expression of contractile proteins concurrent with enhanced collagen expression, both of which could be reversed with TGF‐β blockade in vitro.