Briefly, the increase in [Ca2+]i that was observed in the CF cells as a consequence of reduced CFTR activity [16], as well as pro-inflammatory signals, can lead to ERK 1/2 activation, which in turn promotes the release of NF-kB from its complex with IkBα through the phosphorylation and subsequent ubiquitination/degradation of the inhibitory protein. The gene discussed is NFKB1; the disease is cystic fibrosis.