Disruption of the airway epithelium with bacteria, viruses, and pollutants causes the initial danger signal that incites cytokine/chemokine secretion from epithelial cells to initiate the Th response.[6] Thymic stromal lymphopoietin (TSLP), an epithelial cell-derived cytokine, plays an important role in the development of the Th2 response in nasal polyps.[7] There remains some discrepancy regarding whether IL-25 and IL-33 levels, other epithelium-derived cytokines/chemokines that promote Th2 inflammation, are increased in NPs.[8–12]. The gene discussed is TSLP; the disease is nasal cavity polyp.