Finally, a very recent study showed that type I IFNs are important for the control of parasite proliferation during experimental mouse infection, in particular by promoting the expression of IFNγ by NK cells, and that the toxoplasmic effector T. gondii inhibitor of STAT transcription (TgIST) allows the parasite to limit the reactivity of cells to type I IFNs by inhibiting the signaling pathway dependent on the STAT1/STAT2 heterodimer [104]. This evidence concerns the gene IFNG and infection.