Indeed, FPR1 is highly expressed in glioblastoma cells, and its activation by agonists released from necrotic tumor cells promotes the nuclear translocation of hypoxia-inducible factor 1 alpha (HIF-1α), which increases the protein expression of vascular endothelial growth factor (VEGF), thereby facilitating angiogenesis and subsequent tumor dissemination [76]. This evidence concerns the gene HIF1A and glioblastoma.