Given the exacerbated pathology and increased mortality in Mtb-infected PD-1-deficient mice, it is plausible that enhancing Mtb-specific T cell IFN-γ production by PD-1 blockade in Mtb-infected individuals could ultimately have detrimental effects, as suggested by recent case reports of reactivation of TB in cancer patients treated with anti-PD-1 immunotherapy (74–76). This evidence concerns the gene IFNG and tuberculosis.