It has been demonstrated that viral infection releases TSLP and IL-25 from nasal polyp epithelial cells to help maintain and amplify the T2 immune response common in CRSwNP (66), and it is reasonable to speculate that downregulation of these genes could affect the function of the nasal mucosal epithelial barrier, increases the risk of viral infection, and participates in the pathogenic mechanism of CRSwNP through the aforementioned mechanisms. This evidence concerns the gene IL25 and nasal cavity polyp.