from our group, examining responses in mouse spleens, has demonstrated that NK cells express high basal levels of STAT4 and that their exposure to type 1 IFNs activates STAT4 (9) . Nevertheless, it has only been possible to identify the type 1 IFN induction of NK cell IFN-␥ production during acute viral infections of STAT1deficient but not of STAT1-complete mice because the concurrent induction of STAT1 by type 1 IFN and/or IFN-␥ negatively regulates the response (6, 9) . These results leave open the intriguing question of why a pathway from type 1 IFN to STAT4 activation under basal NK cell conditions would be evolutionarily preserved when it is rapidly turned off at times of type 1 IFN production.