Taken together, these data show that the presence of STAT1α in NK cells and/or accessory cells is required for full-fledged NK cell-mediated tumor growth control and target cell rejection, modestly increases IFNγ production in response to NK1.1 and NKp46 activation and does not impact on IFNγ production in response to IL-12/IL-18 or PMA/ionomycin. Here, IFNG is linked to neoplasm.