STAT1 and infection: Patients have high titers of serum anti-IFN-γ autoAbs, which can inhibit signal transducer and activator of transcription 1 (STAT1) phosphorylation and interleukin-12 production, resulting in severe dysfunction of the Th1 response [2–4] and increased risk of infection by multiple intracellular pathogens, including nontuberculous Mycobacterium (NTM), Talaromyces marneffei (T. marneffei), Cryptococcus neoformans, and other intracellular pathogens [1–12].