Ingestion of a meal is accompanied by gastric secretion that tends to collect immediately below the LES forming an “pocket” or layer of unbuffered acid overly­ing an ingested meal.In health, the transition from the acid to alkaline milieu occurs at the EGJ in the post prandial period [16]. However, when the EGJ barrier is weak or disrupted (e.g. in presence of hiatus hernia) the acid pocket can migrate into the distal esophagus, leading to pathological acid reux in the distal esophagus [17]. Delayed gastric emptying [18] and acid hypersecretory states are additional down­stream factors that can contribute to the esophageal reux burden. At the same time, gastric lling is accompanied by a decrease in LES pressure and an increased fre­quency of spontaneous, transient LES relaxations (TLESRs) that allow air swal­lowed during the meal to be released (belching). Together, these events represent a major challenge to the EGJ reux barrier and it has been shown that when the EGJ barrier is weak or disrupted, especially in the presence of hiatus hernia, the acid pocket can migrate into the distal esophagus, leading to pathological acid reux and mucosal disease [19]. A small number of reux events during TLESRs after meals is normal in healthy individuals; however, the number of reux events is much higher in GERD patients. Studies using magnetic resonance imaging combined with high-resolution manometry (HRM) have shown how active contraction of the clasp and sling bers maintains an acute angle of insertion between the esophagus and the proximal stomach (termed “angle of His” in surgical studies) [20, 21]. The presence of an acute angle of insertion allows the proximal stomach to compress the EGJ and prevents reux of gastric contents into the esophagus [22]. This “ap­valve” effect is much less efcient if the angle of insertion is wide (obtuse) due to ineffective contraction of the clasp and sling bers or structural disruption of EGJ anatomy, both of which are observed in GERD patients [20].