GBM and other highly vascular tumors characteristically overproduce vascular endothelial growth factor (VEGF), which, in addition to promoting angiogenesis, inhibits the secretion of lymphocyte-attracting chemokines like CXCL10 and CXCL11 (69) and downregulates tumor endothelial cell expression of adhesion molecules like ICAM-1 and ICAM-2, VCAM-1 and CD34 (70). Here, VCAM1 is linked to neoplasm.