In alignment with an emerging model of GERD pathogenesis, mediated by inflammatory insult rather than caustic acid-induced injury [62], interleukin-8 (IL-8), a neutrophil chemoattractant and nexus of cell signaling networks regulating proliferation, apoptosis, epithelial-mesenchymal transition, and migration, appears to play a key role in the peptic injury of the larynx and esophagus [8,44,53,63,64]. This evidence concerns the gene CXCL8 and gastroesophageal reflux disease.