 The development of ROP is largely dependent on vascular endothelial growth factor VEGF. When an infant is born prematurely the relatively hyperoxic environment the baby is introduced to shuts down the production of VEGF. Retinal maturation is delayed. Subsequently, at a time when intraocular VEGF levels would normally be declining late in the third trimester of pregnancy, abnormally high levels of VEGF are seen due to large areas of avascular retina and associated tissue hypoxia. The availability of FDA-approved drugs for anti-VEGF treatment renders it possible to treat such eyes off-label. Available drugs include pegaptanib sodium Macugen for partial blockage of VEGF-A, or drugs such as ranibizumab Lucentis and bevacizumab Avastin, which cause complete blockage of VEGF-A. As VEGF is required in the developing retina for normal angiogenesis, our goal is not to penetrate tissue, but to block the excessive levels of VEGF trapped within the overlying vitreous which is responsible for the abnormal vasculature in ROP. 