Given the protective function of IL-1 in early immunity to TB, and the development of type I interferon-mediated disease in hosts with defective IL-1 signaling, e.g., C3HeB mice and Sp140-/- mice in the BL/6 background that phenocopy the susceptibility of C3HeB mice [44,55], the results observed in IL-1R1-deficient mice treated with the FAO-blocking reagent, Mil, are particularly important (Fig 5). The gene discussed is IL1B; the disease is tuberculosis.