IFN-γ secreted by Th1 is critically involved in both antiviral and anti-tuberculosis responses, and it is known that STAT1 is a core mediator of interferon signaling (31), while STAT3 can be upregulated by HIV infection and activated by IFN-γ, promoting the secretion of IL-6 and IL-10, which drive chronic inflammation (32, 33). The gene discussed is STAT1; the disease is tuberculosis.