Recent studies demonstrating the presence of distinct pro-inflammatory mediators such as CRSwNP tissue IL-5, IL-17, and IFN-γ, myeloperoxidase, eosinophilic cationic protein, and IgE in homogenates of CRSwNP tissue support the concept of distinct T cell subsets and consecutive variations in inflammatory patterns in patients with CRS [11, 29, 51]. The gene discussed is IL5; the disease is chronic rhinosinusitis with nasal polyps.