Therefore, treatments targeting these non-conventional checkpoint receptors on Vγ9Vδ2+ T cells (KIRs, ILT-2, and NKG2A) to disrupt the interactions with their respective HLA class I ligands on tumor cells (HLA-C, HLA-G, and HLA-E) may help to enhance the effectiveness of Vγ9Vδ2+ T cell-based tumor immunotherapy. This evidence concerns the gene KLRC1 and neoplasm.