In the absence of correlates, as is the case with protection against TB,15–17 several strategies have been leveraged to date that target TLR receptor signaling, including TLR4 and TLR9 agonists which help drive canonical T-helper 1 (TH1) biased immunity and proinflammatory cytokine responses like interferon gamma (IFN-γ).18 This evidence concerns the gene IFNG and tuberculosis.