Molecularly defined groups of colorectal cancers such as microsatellite instability (MSI)-high tumors and cancers with alterations in the receptor tyrosine kinase/KRAS/BRAF pathways, such as KRAS/NRAS or BRAF mutations and ERBB2 amplifications, may benefit from targeted therapies [4,5,6]. This evidence concerns the gene BRAF and colorectal cancer.