Taken together, our data suggest the possibility for ImmTAB-inhA molecules to recruit multiple T cell subpopulations with broad effector capacities to the sites of infection in TB patients and therefore induce local antimicrobial immune-mediated functions including the elimination of Mtb-infected cells (6) and the T cell–dependent activation of phagocytic cells (65). The gene discussed is INHA; the disease is tuberculosis.