We previously showed that p16INK4A, E-cadherin, hMLH1 and 14-3-3sigma are all inactivated in gastric cancers by promoter hypermethylation (Suzuki et al, 1999, 2000), and that methylation of p16INK4A and hMLH1 is frequently detected in colorectal and gastric cancers associated with the CpG island (CGI) methylator phenotype (Toyota et al, 1999a,b). Here, CDH1 is linked to gastric cancer.