Hence, it is suggested that mutated FBN1 fails to bind to TGF-β, leading to TGF-β overexpression, which in turn promotes the development of AA.53 However, a different view has been proposed because in the mouse model of Marfan’s syndrome, an increase in TGF-β levels in the aorta was not found. Here, TGFB1 is linked to Marfan syndrome.