IL-33, IL-25, and thymic stromal lymphopoietin (TSLP) contribute to the development of inflammation by activating Th2 cells to release Th2 cytokines (e.g., IL-4, 5, 9, 13), which leads to eosinophilia, mast cell degranulation, and mediator release, among other processes, in the large, complicated asthma pathogenic network [68]. The gene discussed is IL25; the disease is asthma.