We observed no IFNγ production in either N. caninum or T. gondii infections in Rag2−/− γC−/− mice (Fig. 5A), and when these data are contrasted with data from RAG1−/− mice, it strongly supports a role for NK cells as being the critical source of early IFNγ during N. caninum infections, and this early response is capable of controlling N. caninum proliferation as early as 4 h post-infection. The gene discussed is RAG1; the disease is infection.