Although hMLH1 hypermethylation is relatively uncommon in EAC compared to gastric, colorectal, or endometrial cancer[32], hMLH1 hypermethylation in BE may cause microsatellite instability in the coding regions of the tumor suppressor genes[33]; 3) a methylator phenotype may be associated with chromatin remodeling[34]; and 4) methylated cytosines are hotspots for mutations, as with the p53 gene[35]. Here, TP53 is linked to Barrett esophagus.