GBM is hypothesized to result from malignant transformation of astrocytes, astrocytic precursors, or neuronal stem cells, and these cells are capable of inducing their own blood supply (25). At initial presentation, it is hypothesized that angiogenesis is largely responsible for neovascularization of GBM. Release of factors such as VEGF, EGF, and FGF from tumor cells stimulates local sprouting of vessels, while recruitment of BMDCs likely plays a minor role. During tumor recurrence after radiation therapy, local sprouting of vessels is largely abrogated, allowing the recruitment of BMDCs to predominate as the main source of neovasculogenesis. In the current issue of the JCI, Kioi et al. (1) identify a potential vasculogenesis pathway whereby hypoxia within the tumor after radiation therapy stimulates HIF-1 release and subsequently elevates SDF-1. Activation of the CXCR4 receptor by SDF-1 promotes mobilization of bone marrow cells, which are then recruited to form new vessels.