However, several contributors have been implicated in the etiology of CRSwNP, including the presence of certain microorganisms, formation of biofilms, bacteria-derived superantigens, dysregulation of the innate and adaptive immunity, and, finally, the presence of asthma and intolerance to the inhibitors of the cyclooxygenase-1 enzyme which together with CRSwNP form aspirin-exacerbated respiratory disease (AERD) [2]. The gene discussed is PTGS1; the disease is chronic rhinosinusitis with nasal polyps.