KLRK1 and glioblastoma: ZOL plays a dual role in GBM immunotherapy by inducing the accumulation of isopentenyl-pyrophosphate, a ligand for Vγ9Vδ2 T cells, while also sensitizing glioblastoma cells to immune attack and increasing the surface expression of NKG2D ligands, rendering glioblastoma cells more susceptible to γδ T cell-mediated cytotoxicity [60,61].