Because PLA2 is an enzyme that catalyses the first rate-limiting step leading to eicosanoids, and specifically sPLA2-X has recently been identified as a potential mediator of AHR in a murine model of asthma and in human subjects with asthma, these findings may reveal a novel mechanism that functionally serves to amplify airway inflammation through the generation of inflammatory eicosanoids known to be increased in the EIB phenotype. This evidence concerns the gene AHR and asthma.