NK cell functional response to tumor cells encounter is triggered by a variety of activating receptors, some of which (e.g., NKG2D and DNAM-1) recognize stress-induced ligands expressed on malignantly transformed cells; additionally, NK cells are potently activated by CD16 or FcγRIIIa (low-affinity Fc receptor for IgG)-dependent recognition of IgG-opsonized targets. This evidence concerns the gene FCGR3A and neoplasm.