Wang et al. [151] showed that patients with BE who progressed from baseline pathology to high-grade dysplasia (HGD) or adenocarcinoma had a significantly higher prevalence of hypermethylation in their initial esophageal biopsies compared to those who did not progress, for both p16 (100% vs. 33%; p = 0.008) and APC (86% vs. 40%; p = 0.02). Here, CDKN2A is linked to adenocarcinoma.