It has been shown to: 1) restore normal pH within phagolysosomes of CF alveolar macrophages; 2) induce neutrophil apoptosis, which is impaired in CF neutrophils; and 3) act as a CFTR modulator by reducing DF508-CFTR degradation and aiding its transfer to the plasma membrane [70]. The gene discussed is CFTR; the disease is cystic fibrosis.