Syndromic TAADs are caused by pathogenic variants in genes associated with the dysfunction of the extracellular matrix and TGF-β signalling and include Marfan syndrome (FBN1), Loeys‒Dietz syndrome (TGFBR1, TGFBR2, SMAD2, SMAD3, TGFB2, TGFB3), Ehlers‒Danlos syndrome (COL1A1, COL1A2, COL3A1, COL5A1 and COL5A2), arterial tortuosity syndrome (SLC2A10), Shprintzen-Goldberg syndrome (SKI) and cutis laxa (EFEMP2, ELN) [12] [14]. The gene discussed is FBN1; the disease is Marfan syndrome.