These models are based on mice exhibiting increased susceptibility to TB as a result of the selection of animals bearing genetic polymorphisms reducing natural immunity (lineages C3HeB/FeJ, DBA/2 or CBA/J), genetic modifications to disrupt key genes associated with host resistance (IFN-γ-, TNF-α- or iNOS- deficient mice), or treatment with TLR- agonists to strengthen the inflammatory response [3–9]. The gene discussed is NOS2; the disease is tuberculosis.