Mutations in genes encoding TGFBR1/2 and SMAD3 are implicated in patients with SCAD and fibromuscular dysplasia (TGF-β), Ehlers–Danlos syndrome (TGF-β1, and TGF-β2 in type IV), Loeys–Dietz syndrome (SMAD2/3, TGFBR1/2), and Marfan syndrome [97,98,99,100]. This evidence concerns the gene TGFBR1 and spontaneous coronary artery dissection.