Double knockout mice with mutations in the type I IFN receptor (Ifnar1 −/−) and Ifn-γ receptor (Ifngr1 −/−) resulted in eschar development in the skin and lethality after intradermal (i.d.)infection of as low as 102 bacteria when compared with 107 when injected intravenously (i.v.), suggesting that IFN signaling in the skin may be important for protective immunity [46,47]. The gene discussed is IFNAR1; the disease is infection.