Indeed, our current findings that IL-18 induced mast cell accumulation, upregulated expression of IL-18R and PAR-2 on mast cells, and Th2 cytokine release in the peritoneum of mice and that tryptase was able to provoke IL-18 release, mast cell accumulation, upregulated expression of IL-18R, and Th2 cytokine release strongly suggested that interactions between IL-18 and tryptase may play a pivotal role in atopic asthma. This evidence concerns the gene IL18 and atopic asthma.