Most antiangiogenesis research has focused on the inhibition of VEGF, which increases in pigment epithelial cells in the early stages of AMD. High concentrations of VEGF in excised CNV and vitreous samples from patients with AMD have further suggested a causal role for VEGF in the initiation of neovascularization. VEGF is a homodimeric glycoprotein that has a heparin-binding growth factor specificity for vascular endothelial cells. It induces vascular permeability, angiogenesis, and lymphangiogenesis, and it acts as a survival factor for endothelial cells by preventing apoptosis. There are at least 4 major VEGF isoforms; VEGF165 is thought to be the most dominant in AMD.