Whether or not the ECs in tumors and in normal tissues are genetically and functionally identical remains controversial (32), even though the tumor endothelium exhibits a phenotype of angiogenically activated ECs in normal tissue, as reflected in the high levels of expression of angiogenic molecules, such as VEGFR, the angiopoietin receptor Tie2, and the adhesive molecules ICAM-1, E-selectin, and CD44 (26). The gene discussed is KDR; the disease is neoplasm.