Accordingly, individuals with inborn errors in the IL‐12/IFNγ axis are highly susceptible to TB, while mice genetically deficient in T‐bet, TNFα, IFNγ, or IL‐12 fail to control bacterial growth [30, 31, 32, 33, 34, 35, 36, 37, 38, 39]. The gene discussed is IFNG; the disease is tuberculosis.