In summary, hyperactivation of NF-κB through both constitutive proinflammatory signaling and/or loss of negative regulation along the GERD–BE–EAC sequence are common routes to providing a prometaplastic and protumorigenic niche; however, the evidence connecting early activation of NF-κB with the occurrence of genetic instability during dysplasia is less clear. This evidence concerns the gene NFKB1 and Barrett esophagus.