The clinical importance of these findings is underlined (a) by the susceptibility of CFTR-deficient individuals to nosocomial pathogens, as observed in cystic fibrosis, (b) by the susceptibility of ENaC-deficient patients who suffer from pseudohypoaldosteronism type I [26] to P. aeruginosa [27, 28], and (c) by the elevated susceptibility of patients with CF-like disease carrying partially dysfunctional CFTR and/or ENaC gene variants to respiratory disease [29]. This evidence concerns the gene CFTR and pseudohypoaldosteronism type 1.