TgIST-dependent attenuation of IFN-γ signaling was demonstrated in bradyzoite-infected fibroblasts (Fig. 7), suggesting that, despite declining levels of TgIST at later time points after infection, the altered chromatin state at STAT1-binding loci may be responsible for long-lasting STAT1 transcriptional repression in the infected host cell. This evidence concerns the gene STAT1 and infection.