Vitreous is vascularized in the fetus but is avascular through normal adult life. This gel changing from a pro-angiogenic to anti-angiogenic milieu accompanies the loss in vasculature. The avascularity of adult vitreous may be due to the myriad of anti-angiogenic proteins normally present that include transforming growth factor-β, pigment epithelial-derived factor, thrombospondin, and endostatin. In disease states such as diabetic and sickle cell retinopathies, preretinal neovascularization grows from retina into vitreous. These angiogenic events occur when there is a shift in balance between angiogenic factors such as vascular endothelial growth factor and anti-angiogenic factors and the vitreous returns to a pro-angiogenic environment.