Previous molecular classification systems have relied on combinations of molecular features, including BRAF, KRAS and TP53 mutation status, microsatellite instability, CpG island methylator phenotype, somatic copy number alterations, and activation of various molecular pathways such as WNT and MYC, in order to classify CRC into subgroups [2–5]. This evidence concerns the gene BRAF and colorectal carcinoma.