It has been reported that methylation of p16 may play a role in the malignant transformation of gastric precursor lesions; p16 methylation was present in 7% IM, in 18% adenomas unassociated with carcinoma, in 29% of adenomas/dysplasias associated with adenocarcinoma and, finally, in 44% adenocarcinomas [103]. This evidence concerns the gene CDKN2A and carcinoma.