In addition, IL-33 has increasingly been implicated in the pathogenesis of a wide range of inflammatory diseases, but particularly in asthma where GWAS studies have demonstrated clear association of the IL-33 and IL-1RL1 genes with human asthma and ST2-deficiency in mice results in suppression of acute eosinophilic inflammation and airway hyper-responsiveness (AHR)1,2. This evidence concerns the gene IL1RL1 and asthma.