We hypothesized that the activated phosphorylated form of IκBα (an inducer of NFκB) would be increased in CF mice exposed to P. aeruginosa LPS or bacteria, and that wt-mice would have lower levels because CFTR was negatively regulating signaling via TNFα-IL-1β-TLR. The gene discussed is NFKBIA; the disease is cystic fibrosis.