C57BL/6 mice deficient in the type I IFN receptor (IFNAR) are indistinguishable from wild‐type mice following M. tuberculosis infection, except for a reduction in splenic bacterial burden.23 However, IFNAR deletion in more susceptible mouse strains substantially improves survival, with mice having much lower bacterial burdens.24, 25 These data from murine models, together with evidence from humans,26 support the notion that type I IFNs are associated with TB disease progression. The gene discussed is IFNAR1; the disease is tuberculosis.