Mechanisms for thelimited efficacy of the adaptive immune response in tuberculosis fall into twogeneral (not mutually exclusive) categories: either the effector functions that Tcells perform (e.g. IFN-γ production) are not effective becauseof failed responses by the infected cells targeted by effector T cells; or the Tcells recruited to the site of infection do not optimally perform the effectorfunctions required for immune clearance. The gene discussed is IFNG; the disease is infection.