Barrett's esophagus (BE) develops as a complication of chronic gastro-esophageal reflux, and its importance is derived from its association with esophageal adenocarcinoma (ACA) [1]. BE is found in 10% of patients with gastroesophageal reflux. It is a premalignant condition and is associated with a risk of esophageal ACA up to 125-fold greater than in the general population [2,3]. The sequence to carcinogenesis is thought to follow a progression from Barrett's metaplasia, through low-grade dysplasia (LGD) and high-grade dysplasia (HGD) and, finally, to ACA [4]. Furthermore, various studies have shown that the overall incidence of ACA from Barrett's metaplasia ranges from 0.2% to 2% [5] and that approximately 32% of patients diagnosed with BE with HGD progress to esophageal ACA within 5 years [6). In addition, several other studies have shown that 38% to 73% of patients who undergo an operation after an endoscopic biopsy diagnosis of HGD already have esophageal ACA [7-16]. The initiation of surveillance programs has led to earlier diagnosis of HGD and early esophageal ACA, which has presumably saved many lives [17-19]. Although the prognosis of ACA is extremely poor (with a 5-year survival rate of 13% to 15%), when esophageal ACA is found in the early stages, it has a good chance of being cured [20,21]. The authors' current management options for BE with HGD include (1) surveillance, (2) endoscopic mucosal ablative therapies, and (3) esophagectomy. In this manuscript, the diagnosis, evaluation, and management of patients with BE with HGD and its relationship with ACA is discussed.