In a pulmonary model of infection with Chlamydophila pneumoniae, NOD2, and RIPK2 were found to be critical for host responses; Nod2- and Ripk2-deficient mice infected with C. pneumoniae exhibited impaired production of nitric oxide and chemokine (C-X-C motif) ligand 1 production and delayed neutrophil recruitment to the lungs (Shimada et al., 2009). This evidence concerns the gene RIPK2 and infection.