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Because vascular endothelial growth factor receptor (VEGFR)-2 activation can lead to nitric oxide induction, we hypothesized that inhibition of VEGFR-2 would lead to morphologic and functional changes similar to direct inhibition of nitric oxide. Pancreatic cancers in nude mice were treated with a VEGFR-2 monoclonal antibody, a nitric oxide synthase inhibitor, or the combination. Mice were injected with Hoechst 33342 (blue) to assess tumor perfusion and sections were stained for CD31 (red). Inhibition of VEGFR-2 and nitric oxide led to distinct vascular morphology and perfusion. Combination therapy led to the greatest decrease in vessel density and perfusion. For further details, please see Camp et al. on page 2628 in this issue.