These data suggest that the somewhat attenuated, and more variable, NK‐cell IFN‐γ responses observed in mice with lethal compared to nonlethal infections might result from limitations in the in vivo availability of IL‐2 as well as reliance on signaling via the low‐affinity (CD122) IL‐2R rather than the high‐affinity (CD25) receptor. The gene discussed is IL2; the disease is infection.