However, CMKLR1-deficient mice had an increased inflammatory response in lipopolysaccharide-induced acute lung inflammation (Luangsay et al., 2009) and had delayed clearance of the virus and a higher mortality, in the pneumonia virus of mice model (Bondue et al., 2011a), as a result of the loss of the anti-inflammatory pathways involving CMKLR1. This evidence concerns the gene CMKLR1 and susceptibility to pneumonia measurement.