The inability to upregulate IFNγ expression (e.g., deficiency in the cytokines IL-12 or IL-18, or their receptors), produce it, or respond to it (e.g., deficiency in the IFNγ receptor chains, Jak2 or Stat1), leads to high susceptibility to experimental mycobacterial infection in mouse models and in humans (45) (Figure 1 “active TB”). The gene discussed is IFNG; the disease is tuberculosis.