To clarify the role of endothelial Notch signaling in tumor angiogenesis, we employed mice with tamoxifen-induced EC-specific NIC overexpression (NICeCA, Cdh5-CreERT-ROSA-Stopfloxed-NIC) or RBPj knockout (RBPj∆E, Cdh5-CreERT-RBPjfloxed) to activate or block canonical Notch signaling in TECs, respectively (Figure S1A-D) 38. The gene discussed is CDH5; the disease is neoplasm.