In some models of severe TB (e.g., C3HeB/FeJ (“Kramnik”) mice [39], Sp140-/- mice [40], and mice depleted of GM-CSF [19]) the excess pathology is largely dependent on dysregulated type I interferon signaling, while in other models (i.e., Nos2-/- and Acod1-/- mice) the excess bacterial burden appears to be independent of type I interferon and has largely been attributed to dysregulated IL1 signaling [41]. The gene discussed is ACOD1; the disease is tuberculosis.