Studies where excess levels of type I IFN are induced during TB, either through direct instillation of IFN-α/β into the lung (18), administration of a polyinosinic-polycytidylic acid derivative (15), or abrogation of a negative regulator of type I IFN signaling (28) support a detrimental role for type I IFN during TB, as they all resulted in exacerbated disease. The gene discussed is IFNA1; the disease is tuberculosis.