CCL5 and glioblastoma: Endothelial cells and GAMs release pro-inflammatory interleukin (IL)-6, which has been implicated in several pro-tumoral processes in GBM; as it enhances the activity of phosphoglycerate kinase 1 (PGK1) by promoting its phosphorylation, it reinforces GBM metabolic dependence on aerobic glycolysis and promotes macrophage recruitment by upregulating CCL5/CXCL5 and supports their alternative activation via PPAR/HIF-2 signaling [46] (Figure 2).