ATM and adenoma: In studies on relapsed colorectal lesions, the promoters of the tumor suppressor genes mutL homolog 1 (MLH1), ataxia telangiectasia mutated (ATM) and fragile histidine triad (FHIT) were found to be significantly hypermethylated in recurring conventional adenomas [27], while the absence of phosphatase and tensin homolog (PTEN) expression correlated positively with local recurrence [28].