The essential role of IFN-γ is evident from the increased risk of tuberculosis in: (i) individuals with deficiency of IFN-γ and interleukin-12, which promotes Th1 cell differentiation; (ii) animal models depleted of CD4+ T-cell during the experimental infection; (iii) HIV-infected individuals [25], [26]. The gene discussed is IFNG; the disease is infection.