Interestingly, the lack of Myct1 in TAECs augmented antitumor immunity, as shown by the enhanced transendothelial migration of cytotoxic T lymphocytes and M1 macrophage polarization in the absence of endothelial Myct1. The combined inhibition of Myct1, programmed death 1 (PD1) and VEGFR2 signaling completely blocked tumor growth, whereas cotreatment with anti-PD1 and anti-VEGFR2 blocking antibodies failed to induce tumor regression. The gene discussed is KDR; the disease is neoplasm.