While immediate biological interpretation of our results is not possible, defects in M. tuberculosis recognition and/or subsequent intracellular signaling in the nuclear factor kappa B (NF-κB) pathway related to TLR2 polymorphisms would be consistent with the subtle innate immune defects in the extrapulmonary tuberculosis patients in this study population: low unstimulated cytokine production, decreased TNF-α production in response to LPS or LPS + IFN-γ, and low CD4+ lymphocytes[6,7,4]. Here, NFKB1 is linked to tuberculosis.