While TIM-3 blockade is reported to restore T cell functions and improve control of bacterial load in chronically infected susceptible mice (9), TIM-3-expressing T cells from patients with pulmonary TB produce the cytokines IFN-γ/tumor necrosis factor alpha (TNF-α)/interleukin-22 (IL-22), and function as effector cells limiting intracellular M. tuberculosis growth in macrophages (26). This evidence concerns the gene HAVCR2 and pulmonary tuberculosis.