Approximately 50% of melanomas and 10% of colorectal cancers (CRC) harbor V600E/K point mutations in the cytosolic kinase BRAF. While receptor-mediated activation of RAS-GTP normally regulates activity of the enzyme by catalyzing the formation of BRAF dimers, V600 mutations result in constitutive signaling by the BRAF monomer, and subsequent MEK and ERK phosphorylation.1 The effector kinase ERK phosphorylates over 100 cytosolic and nuclear substrates, which regulate enzymatic activity and gene expression, promoting cell proliferation and survival.2 This evidence concerns the gene BRAF and colorectal cancer.