The ability to rapidly activate innate immune responses is likely to be critical in the containment of mycobacteria during primary infection in childhood, as evidenced by the unique susceptibility to mycobacteria in patients with Mendelian defects in interferon gamma (IFNγ) and interleukin 12 (IL-12) pathways [9], [10], [11], [12]. The gene discussed is IFNG; the disease is infection.