In wild-type mice, after infection and INH and RIF treatment, anti-IL-17A antibody treatment for four weeks did not induce any signs of inflammation or reactivation of infection (Fig. 3C,D), whereas TNFα-deficient mice and Enbrel (TNFα-neutralizing TNFR2 fusion molecule)-treated mice showed marked to moderately increased levels of mycobacterial burden, respectively. The gene discussed is TNF; the disease is infection.