Since overexpressed HLA-E can prevent tumor cell lysis mediated by Vδ2 T cells, the blockade of the NKG2A-HLA-E axis may enhance the Vδ2 T cell-based immunotherapeutic efficacy by administering anti-NKG2A/CD94 mAb to unleash Vδ2 T effector functions. Here, KLRC1 is linked to neoplasm.