Although the baseline activities of acid Sphingomyelinase and acid Ceramidase in lung homogenates from CFTR deficient animals are equivalent to those in control mice [91], they achieved partial inhibition of the activity of acid Sphingomyelinase either by intraperitoneal injection of amitriptyline or by heterozygous deficiency for acid Sphingomyelinase and observed reduced airway inflammation, phagocyte recruitment, and susceptibility to infection by Pseudomonas aeruginosa [91, 111]. The gene discussed is CFTR; the disease is infection.