The mechanisms of peptic injury during GERD and LPR demonstrate significant overlap with the known biological functions of E-cadherin RIP fragments: hyperproliferation, dysregulated cell migration, altered wound healing, EGFR activation, change in cell phenotype, and apoptotic resistance [65,74,75,91,92,93,97,98,99]. The gene discussed is EGFR; the disease is gastroesophageal reflux disease.