Editorial

Wild-type KRAS acts as a switch during signal transduction; how-ever, somatic mutations that activate regulators and effectors of Ras proteins are common in tumor development and cancer [1-3]. In approximately 35%–42 % of early colorectal cancer (CRC) pa-tients, the KRAS mutation inhibits KRAS GTPase, resulting in a constitutive KRAS activation and, thus, activating a Ras/Raf signal-ing pathway. In CRC, 97 % of KRAS mutations occur in codons 12 and 13 of exon 2, and more than 97 % of changes in the protein are attributable to changes in the amino acid sequence by the substitu-tion of seven DNA base pairs [4]. BRAF is a human gene that en-codes the protein B-Raf, which is considered a proto-oncogene, encoding a serine/threonine protein kinase [5]. B-Raf is a member of the Raf kinase family that regulates the Ras/Raf/MEK/extracel-lular signal regulated kinase (ERK) pathway and is involved in di-vision, differentiation, and secretion [6]. The most common BRA