Therefore, genetic modification of (γδ)T-cells, naturally expressing the NKG2D receptor, were genetically modified and expanded ex vivo with an MGMT-expressing lentivector that provided resistance to TMZ, allowing therefore the simultaneous infusion of (γδ)T-cell with chemotherapy, and targeting therefore the tumor when NKG2DL are maximally expressed (Figure 2C). This evidence concerns the gene MGMT and neoplasm.