The increased branching and tortuosity of tumor blood vessels in the SS.BN3IL2Rγ- hosted (low-DLL4) tumors fits with previously reported data demonstrating that pharmacological inhibition of DLL4 attenuates tumor growth and progression by eliciting nonproductive angiogenesis (i.e., a higher density of poorly functioning vasculature) 31-34. This evidence concerns the gene DLL4 and neoplasm.