Two cytokines are known to be critical for humans to control tuberculosis: IFN-gamma, as judged by the predisposition to mycobacterial infection in people with genetic deficiency states in proteins involved in IFN-gamma production and signaling [31], and TNF-alpha, as revealed by the risk of reactivation of latent tuberculosis infection in people given therapeutic agents that neutralize TNF-alpha in the treatment of inflammatory diseases [32]. The gene discussed is IFNG; the disease is tuberculosis.