Similar susceptibility to Listeria monocytogenes infection was observed in IFNAR−/− mice, together with a decreased splenic apoptosis [250], while increased resistance to intradermal infection with Francisella tularensis (the etiologic agent of tularemia) in these deficient mice was associated with an expansion of IL-17+ γ/δ T cells and neutrophils [251]. The gene discussed is IL17A; the disease is infection.