Somatic KRAS mutations are detected in about 40% of colorectal cancer and lead to an abnormal affinity of KRAS for GTP with permanent activation of the transduction cascade. KRAS mutations have been identified as a reliably strong negative predictive factor to anti-EGFR monoclonal antibody therapies in mCRC patients [2–4]. KRAS mutation screening has been mandatory in Europe since July 2008 and aims to restrict treatment of mCRC to cetuximab and panitumumab in patients with wild-type KRAS tumors [5, 6]. This evidence concerns the gene EGFR and colorectal cancer.