A direct consequence of this CFTR defect is that the salt concentration within the lungs of CF patients is higher than in healthy individuals (Smith et al., 1996) and this high salt concentration has been shown to inhibit the antibacterial activity of natural HDPs like HNP1 (Turner et al., 1998) possibly contributing to increased susceptibility to bacterial infections. The gene discussed is CFTR; the disease is cystic fibrosis.