TNF inhibitors have been linked to TB reactivation, emphasizing the role of TNF in MTb control. The reduction in CXCR3 expression, the possibility of MAIT cells homing to inflamed kidney tissues, and the shift in cytokine production away from IFN/TNF and toward GM-CSF all likely contribute to an immune environment more receptive to MTb infection and reactivation. This evidence concerns the gene TNF and tuberculosis.