Although the exact molecular pathophysiology of MFS-associated aortic widening is not completely understood, the progressive nature of the disease is generally accredited to the structural abnormality of FBN-1 microfibrils leading to perturbation of the TGF-β signaling cascade and the upregulation of downstream MMPs which contribute to medial degeneration observed in MFS15. Here, FBN1 is linked to Marfan syndrome.