Redundant mechanisms of postnatal neovascularization. Based on the studies outlined herein, we postulate that redundant mechanisms exist to achieve postnatal neovascularization. Within BM and other tissues including blood vessels, reside cells that are capable of participating in new blood vessel formation. Examples of these cell types and their phenotypes are provided. The extent of contribution is dependent on the model system. Some models including injured retinas (red circle) demonstrate robust BM contribution resulting in entire BM-derived blood vessels. Other models like LLC tumors (purple tumor) will incorporate BM cells into new vasculature, but the microenvironment of the tumor may also use other means of tumor neovessel formation. In this setting, redundant mechanisms act in concert to achieve new blood vessel growth. Finally, models such as B16 tumors (blue tumor) will have little to no BM contribution and rely mainly on non–BM-derived cells to generate new vessels. At sites of neovascularization, SDF-1α acts as a regulatory molecule necessary for BM recruitment and participation. Active sites that do not express SDF-1α are much less prone to BM involvement and undergo neovascularization via a non–BM-derived mechanism.