As both serum IgE and blood eosinophil count were shown to be independent risk factors for comorbid asthma in CRSwNP patients, this suggests that this disease may possibly be due to enhanced activation and interaction of two branching pathways of type 2 inflammation; i.e. Interleukin (IL)-5/eosinophilic and IL-4/IL-13/IgE. The gene discussed is IL4; the disease is asthma.