CFTR and cystic fibrosis: Importantly, inhibition of GSK-3β, a key component of the β-catenin degradation complex determining the fate of β-catenin, in CF mice and Caco-2 cells rescued β-catenin activity and suppressed the CFTR dysfuction-induced NF-κB/COX-2/PGE2 activity (Figure 4A–4E), suggesting that β-catenin may serve as an inhibitor of the NF-κB-mediated inflammatory response.