These data indicated that wild-type CFTR (wt-CFTR) has inherent anti-inflammatory properties that suppress baseline and stimulated NF-κB mediated inflammatory signaling in bronchial epithelial cells, while in CF abnormal CFTR function contributes to generally increased inflammation via disrupted suppression of the NF-κB pathway (Vij et al., 2009; Hunter et al., 2010). This evidence concerns the gene NFKB1 and cystic fibrosis.