Wild-type and Stat1-L351F knock-in mice were challenged intranasally with T. marneffei and analyzed for lung fungal burden, histopathology, immune profiling, and bulk lung transcriptomics; infected Stat1-L351F mice additionally received ruxolitinib to probe the impact of JAK inhibition on infection-associated myeloid responses.<h4>Results</h4>The proband displayed an interferon-skewed cytokine milieu, and patient PBMCs supported increased ex vivo growth of T. marneffei and C. neoformans, whereas C. albicans did not show a consistent increase. Here, STAT1 is linked to infection.