The migration of lymphocytes to tumor sites is essential for immune surveillance, and therapies that enhance lymphocyte adhesion and infiltration, such as combinations of anti-VEGFR2 and anti-PD-L1 antibodies, which activate lymphotoxin-beta receptor (LTbR) signaling and lead to the formation of high endothelial venules (HEVs), are being studied for their ability to boost the tumor immune response (94, 95). The gene discussed is KDR; the disease is neoplasm.