Nowadays two main independent molecular pathways of colorectal tumorigenesis have been proposed: the conventional adenoma-carcinoma pathway characterised with the initial inactivation of the APC gene, accumulation of mutations in other genes and chromosomal instability [46]; and the serrated pathway with microsatellite instability, a relatively high frequency of BRAF mutations and increased level of DNA methylation [47]. This evidence concerns the gene BRAF and carcinoma.