This heterogeneity is increasingly recognized as resulting from distinct molecular subtypes of colorectal cancers,[2] which in turn is influenced by the molecular pathway of carcinogenesis through which cancer develops in individuals.[3] For example the prognosis of patients whose cancers develop through the chromosomal instability pathway differs from those who develop colorectal cancer through germline loss of mismatch repair enzymes, which differs from the poor prognosis of patients with cancers characterized by the CpG island methylator phenotype and BRAF V600E mutation.[4], [5]. This evidence concerns the gene BRAF and cancer.