Given that IFN-γ-STAT1 signaling serves as a dominant pathway driving immune activation and host defense during intracellular parasitic infection [28–31], we focused our efforts on evaluating (i) how microglial Stat1 deletion impacts host susceptibility to T. gondii, (ii) the systems-level effects of this deletion during T. gondii challenge, and (iii) a potential role for STAT1 signaling in regulating DAM activation during infection. This evidence concerns the gene IFNG and parasitic infectious disease.