Further, HNPCC and sporadic MSI-H cancers have distinct histological and molecular features: While, both cancer types display lymphocytic infiltration, mucin secretion and poor differentiation [67], HNPCCs tends to originate from classical adenomas compared to sessile-serrated adenomas in the case of MSI-H CRCs [68]; on a molecular level, HNPCCs are strongly associated with mutations in APC or ß-catenin and/or KRAS [67,68], while MSI-H sporadic CRCs instead exhibit BRAF mutations, which are present in CRC precursor lesions [68]. This evidence concerns the gene KRAS and adenoma.