In addition, abnormally expressed IL-36 family cytokines were detected in patients with chronic rhinosinusitis with nasal polyps (CRSwNP), the refractory form of which is believed to be associated with increased IL-36α concentration as a risk factor [13], while IL-36γ promoted the secretion of chemokines and adhesion factors and induced neutrophil infiltration [14]. This evidence concerns the gene IL36A and chronic rhinosinusitis.