Upon tumor transformation or viral infection, cells lose, in part or completely, HLA-I expression, thus evading CTL recognition, and upregulate/express de novo ligands for activating NK cell receptors (i.e., NKp30, NKp44, NKp46—referred to as Natural Cytotoxicity Receptors or NCRs, NKG2D, activating KIRs—aKIRs, NKG2C, DNAM-1), hence becoming targets for the killing activity of NK cells in which triggering signals have prevailed. This evidence concerns the gene KLRK1 and neoplasm.