Once patients with CF are challenged by bacterial or viral infection, airway inflammation is disproportionate to the degree of infection, with a high PMN infiltration and large release of pro-inflammatory molecules, such as tumor necrosis factor (TNF)-α, interleukin (IL)-8, 6, 1β (Balough et al., 1995; Bonfield et al., 1995; Noah et al., 1997; Muhlebach et al., 1999; Tirouvanziam et al., 2000; Muhlebach and Noah, 2002), prostaglandins, and LTB4 (Konstan et al., 1993). The gene discussed is TNF; the disease is infection.