By eliminating the availability of VEGF, intraocular anti-VEGF therapies are effective for wet age-related macular degeneration (AMD), which is characterized by the presence of choroidal neovascularization.1 Using either antibodies (such as Lucentis, Avastin) or soluble decoy receptors (such as Eylea), current anti-VEGF therapies target the interaction between VEGF and its receptors, but not endogenous VEGF expression. This evidence concerns the gene VEGFA and choroidal neovascularization.