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Destruction of existing tumor blood vessels may be achieved by targeting vascular endothelial growth factor (VEGF) signaling, which mediates not only endothelial cell proliferation but also endothelial cell survival. In this study, however, intravital microscopy failed to demonstrate that targeting of VEGFR‐2 (by the tyrosine kinase inhibitor SU5416) induces significant regression of experimental tumor blood vessels. Immunohistochemistry, electron microscopy, expression analyses, and in situ hybridization provide evidence that this resistance of tumor blood vessels to VEGFR‐2 targeting is conferred by pericytes that stabilize blood vessels and provide endothelial cell survival signals via the Ang‐1/Tie2 pathway. In contrast, targeting VEGFR‐2 plus the plate‐let‐derived growth factor receptor (PDGFR)‐β system (PDGFR‐β signaling (by SU6668) rapidly forced 40% of tumor blood vessels into regression, rendering …