Consistent with our hypothesis, our data showed that IFN-γ mRNA levels were down-regulated in both the LTBI group and the active TB group compared with the healthy controls, and IFN-γ mRNA expression was decreased more in the active TB group compared with the LTBI group, which could partly explain one mechanism that overexpressed miR-29 in the active TB group might inhibit CD4+ T cells response to TB infection by suppression of IFN-γ–mediated signalling pathway. Here, IFNG is linked to tuberculosis.