In our case, we postulate that the acidic gastric content was constantly passing through the fistulous tract that induced esophageal hypersensitivity and triggered the onset of dysphagia and worsening heartburn symptoms. In other words, gastric acidic content had two routes of passage: the native gastro-esophageal (GE) junction and the EGF. Our patient responded well to conservative management with PPIs along with successful closure of the EGF; Hence, endoscopic therapy and surgical repair were spared. To the best of our knowledge, resolution of EGF without endoscopy or surgery has not been documented yet in medical literature.