The somatic mutations commonly occur at positions G12 or G13 of KRAS and V600 of BRAF. Amplification and activating mutations of receptor tyrosine kinases such as EGFR are also frequently implicated in the aberrant activation of the RAS/RAF signaling cascade in CRC, with additional evidence that RAS mutations result in resistance to anti-EGFR therapy [4]. This evidence concerns the gene RAF1 and colorectal carcinoma.