TB has often been thought to primarily result from loss of immune control, because approximately 90% individuals infected with TB never progress to active disease, and this progression is increased in the context of immune deficiency; such as in cases of HIV infection, in infants, people with genetic deficiency of the IL-12/IFN-γ signalling pathway or after anti-TNF-α antibody treatment (O'Garra et al., 2013). Here, TNF is linked to tuberculosis.