A cause-and-effect relation between gastroesophageal reflux disease and Zenker diverticulum remains unclear. Convincing evidence exists demonstrating that patients with Zenker diverticula have increased resting tone of the cricopharyngeus muscle, and that this may be an important initiating factor for the development of Zenker diverticula. Yet some patients with cricopharyngeus hypertonicity never develop Zenker diverticulum. In this context, we hypothesize that acid-induced esophageal shortening may be an important cofactor. We suggest that acid reflux induces longitudinal esophageal shortening, which in turn increases the risk for the development of herniation between 2 spatially related structures, the pharyngeal constrictors and cricopharyngeus muscles, leading to the development of Zenker diverticulum. This hypothesis awaits clinical verification.