The uptake of glioblastoma (GBM) cell-derived EVs to the recipient GBM cells were shown to involve a triple interaction between the chemokine receptor CCR8 on the cells, glycans exposed on EVs and the soluble ligand CCL18, which in turn promoted GBM cell proliferation and resistance to the alkylating agent temozolomide [63]. This evidence concerns the gene CCL18 and glioblastoma.