Most cases of CRSwNP share the same pathogenesis with severe asthma, which is characterized by T helper 2 (Th2) cell-biased inflammatory reactions, eosinophilia, and immunoglobulin E (IgE) hyperproduction, in which IgE plays a crucial role in stimulating related type 2 inflammatory cells, such as mast cells, basophils and eosinophils.14 This evidence concerns the gene IGHE and chronic rhinosinusitis with nasal polyps.