Thus, the authors suggested that the mucosal epithelial barrier is compromised in the context of CRS disease, especially CRSwNP, and that loss of AQP5, which might act as a tight junction protein, plays a role in the development of mucosal edema and the pathophysiology of nasal polyp formation [57]. The gene discussed is AQP5; the disease is chronic rhinosinusitis with nasal polyps.