The persistent NF-κB activation in human CF airway cells is the consequence of the synergistic effects of bacterial components, such as flagellin, where flagellin interacting with asialoGM1 receptor favors the release of ATP from CF airway cell lines, which mediates purinergic receptors and activates downstream intracellular Ca2+ signaling that synergizes with the TLR5-dependent signaling to activate NF-κB (see section host-pathogen interactions and intracellular signaling modulating IL-8/CXCL8 expression) (92). The gene discussed is NFKB1; the disease is cystic fibrosis.