Possible CFTR/TWIST1 bridging pathways include: (1) β-catenin, which interacts with both CFTR52 and TWIST153 in EMT contexts; (2) transcription factor hypoxia-inducible factor 1α (HIF1α) implicated in CF pathophysiology54 and a known TWIST1 regulator55; and/or (3) NF-κB, an important player in CF56 also associated with TWIST157. The gene discussed is NFKB1; the disease is cystic fibrosis.