However, in CF airways challenged by bacteria or viruses, inflammation appears disproportionate to the degree of infection, with a high PMN infiltration and release of pro-inflammatory molecules, such as TNF-α, IL-8, IL-6, IL-1β, proteases, oxidants, PG, and LT, together leading to bronchiectasis and fibrosis (Konstan et al., 1993; Balough et al., 1995; Bonfield et al., 1995; Khan et al., 1995; Noah et al., 1997; Muhlebach et al., 1999; Tirouvanziam et al., 2000; Muhlebach and Noah, 2002). The gene discussed is TNF; the disease is cystic fibrosis.