Additional GERD/EAC-relevant molecules that undergo RIP include LRP1 (putative pepsin receptor [89]), TNFA, OPA1 (whose RIP results in apoptotic resistance and mitochondrial cristae remodeling [90] similar to that induced by pepsin [91,92,93]), CD44 (adhesion molecule elevated in esophageal cancer [94]), EpCAM (adhesion molecule and prognostic indicator of esophageal cancer [95]), and Notch (role in EAC [96]). This evidence concerns the gene CD44 and gastroesophageal reflux disease.