SeNPs have been shown to potentiate the antitumor activity of γδ T cells in breast cancer through the stabilization of the microtubule network, the upregulation of the expression of cytotoxicity-related molecules (NKG2D, CD16 and IFN-γ) and the downregulation of the immunosuppressive PD-1 expression in these cells. This evidence concerns the gene KLRK1 and breast cancer.