By challenging ITK-deficient leukocytes (obtained long after the clinical remission of TB) with BCG, we demonstrated profoundly impaired IL-23-dependent IFN-γ production by MAIT and Vδ2+ γδ T lymphocytes, two well-established IFN-γ–producing lymphocyte subsets (Le Bourhis et al., 2010; Chen, 2016), and partially impaired IFN-γ production by CD4+, CD8+, and DN αβ T lymphocytes. Here, ITK is linked to tuberculosis.