The clinical implication of these findings is that treatment of CF patients with small molecule or therapeutic compounds that rescues optimal amount of mutant CFTR to the cholestrol-rich cell surface lipid rafts can inhibit the NFκB mediated chronic inflammation and rescue the pathology induced by defective CFTR, potentially attenuating the progression of CF or related obstructive lung diseases like COPD and emphysema. The gene discussed is CFTR; the disease is pulmonary emphysema.