To determine the common molecular mechanisms of increased angiogenesis in SFD, we expressed three of the known SFD TIMP3 mutations (S179C-TIMP3, Y191C-TIMP3 and S204C-TIMP3) in endothelial cells to evaluate if the glycosylation state of the protein plays a role in the increased VEGF-mediated angiogenesis phenotype. The gene discussed is TIMP3; the disease is Sorsby fundus dystrophy.