While tubular adenomas are more commonly thought to be stimulated by genomic instability through suppressing the APC gene in addition to chromosome instability, premalignant serrated polyps are correlated with epigenetic alterations through the CpG island methylator phenotype, which represents aberrant hypermethylation of CpG dinucleotides underlining the heterogeneity of CRC and the involved genetic and epigenetic instability levels[3]. This evidence concerns the gene APC and colorectal carcinoma.