BRAF and carcinoma: This proposal subsequently received strong support through the demonstration of molecular alterations common to both types of serrated polyp, notably mutation of BRAF and extensive DNA methylation.12 This viewpoint was consolidated through the formal recognition of two largely independent pathways of colorectal tumorigenesis: (i) the traditional adenoma–carcinoma sequence associated with chomosomally unstable CRCs,13 and (ii) the ‘serrated pathway’ culminating in CRCs with DNA microsatellite instability (MSI), mutation of BRAF and extensive DNA methylation.12,14–20