From a pathophysiological view, both disorders, CRSwNP, and asthma share the same type 2 immunopathology (involvement of IgE, eosinophils, interleukin-4 (IL-4)/IL-13, and IL-5) and exhibit epithelial barrier dysfunction [16–21]. This evidence concerns the gene IL13 and chronic rhinosinusitis with nasal polyps.