However, the role of aberrant methylation in the aetiopathogenesis of HNPCC remains questionable: Kaz et al. found promoter methylation of MLH1 in 53% of HNPCC adenomas [60], compared to only 4% of sporadic adenomas, whilst Speake et al. found 40% and 25% of hyperplastic polyps of sporadic or HNPCC origin to be CIMP-H [61]. This evidence concerns the gene MLH1 and hyperplastic polyp.