TSLP, but not IL-25 and IL-33, was constantly upregulated in eosinophil-rich areas (nasal polyps) of ECRS when compared with eosinophil-poor areas (uncinate tissues of the same patients), and was significantly enhanced by co-incubation with eosinophils or EPX in BEAS-2B cells, suggesting eosinophilic inflammation induced TSLP, consistent with a previous report [15]. This evidence concerns the gene TSLP and nasal cavity polyp.