The vessel defects induced by the Dll4/Notch inhibition closely resemble vascular abnormalities commonly observed in human malignancies; so increased Dll4 expression in tumor vasculature, that reduces endothelial sensitivity to VEGF [32], may be considered a host defense mechanism serving to restrict tumor vascularization and malignant cell access to the bloodstream such as Angiopoietin-2 does in the case of vascular cooption [33]. Here, ANGPT2 is linked to neoplasm.