NFKB1 and gastroesophageal reflux disease: PKAc in the activated IκB-NF-κB-PKAc complex phosphorylates p65, inducing further formation of p50/p65 heterodimers, which translocated to the nucleus to stimulate transcription of NF-κB p50 target genes(e.g.CDX2) that might play a role in columnar metaplasia [62], one of the pathophysiological mechanisms of GERD.