The endogenous bronchodilator, S-nitrosoglutathione (GSNO) has been proposed as a possible pharmacological remedy that reverses the CFTR-ΔF508 maturation defect as detected by immunoblot [11], causes a 4-fold increase in CFTR-mediated chloride efflux and promotes apical location of CFTR in cultured CF airway epithelial cells [12]. Here, CFTR is linked to cystic fibrosis.