An improved understanding of the underlying disease pathophysiology of Type 2 inflammation, which is characterized by the presence of eosinophilic airway inflammation associated with IL-4, IL-5, IL-5Rα, IL-13 and circulating or local IgE, has led to new developments in medical management of CRSwNP that are aimed at modulating the Type 2 inflammatory response [2]. The gene discussed is IGHE; the disease is chronic rhinosinusitis with nasal polyps.