However, this is a double edged sword as the reduction of the pro-inflammatory IFN-γ in hyperglycemia not only slows down the inflammation-based pathology of TB but also hinders killing of the bacteria, induction of nitric oxide synthesis, and macrophage activation that depend on IFN-γ (Etnaet al., 2014). The gene discussed is IFNG; the disease is Hyperglycemia.