On the basis of these results, we proposed that the targeting antibodies (e.g. αPD-L1) on the cell surface first facilitates binding of γδ T cells to the targeted cancer cells via binding to the tumor antigens (e.g. PD-L1), which induces the interactions between γδ TCR and BTN3A1/2A1, co-stimulation receptors and ligands, and death ligands and receptors. The gene discussed is BTN3A1; the disease is neoplasm.