Nitric oxide (NO) produced by macrophages after cell activation by IFN-γ hampers the growth of CP[26], and these findings are consistent with the delayed IFN-γ production observed in Casp1−/− mice (Figure 1C), supporting a model whereby IL-1β secretion by AM induces early IFN-γ that, in turn, activates AM at the infection site to induce iNOS and clear CP. Here, CASP1 is linked to infection.