Activation of VEGF-A RTKs, such as VEGFR-1 (Fms-like tyrosine kinase 1) and VEGFR-2 (kinase insert domain receptor in humans; fetal liver kinase 1 in mice), which are expressed in tumor and stromal peritumoral cells [154,162,163], plays a vital role in GBM angiogenesis from regions adjacent to the pseudopalisade with a high vascular density [81]. The gene discussed is VEGFA; the disease is neoplasm.