However, in some murine models of severe TB such as Nos2-/- and Acod1-/-, the susceptibility is independent of type I interferon signaling despite the fact that dysregulated neutrophil responses also play a detrimental role in these strains [16,17,41], suggesting that the impact on disease severity may depend on the detailed mechanisms by which susceptibility arises in each background. This evidence concerns the gene NOS2 and tuberculosis.