Yet, this therapy provided moderate clinical benefits with stable disease being the mostly outcome for patients who respond to this therapy (7).One of the reasons for this suboptimal effectiveness is the hostile tumor microenvironment that negatively regulates the anti-tumor functional characteristics of Vγ2Vδ2 T cells by the engagement between the programmed death-ligand 1 (PD-L1) expressed on the tumor cells and PD-1 expressed on the Vγ2Vδ2 T cells (8). Here, CD274 is linked to neoplasm.