Models of staphylococcal pneumonia in mice lacking components of innate immune signaling, such as the type I IFN receptor null (Ifnar-/-) mice [12, 13], tumor necrosis factor receptor 1 null (Tnfr1-/-) mice [14], type III interferon (IFNλ) receptor null (Il28r-/-) mice [15] or nucleotide-binding oligomerization domain-containing protein 2 null (Nod2-/-) mice [16], have significantly improved outcomes. This evidence concerns the gene NOD2 and staphylococcal pneumonia.