Although the epidermal growth factor receptor (EGFR) has become an important therapeutic target for CRC treatment, approximately 40% of patients with metastatic colorectal cancer (mCRC) have tumours with KRAS mutations, which are not expected to respond to anti-EGFR therapies.1,2 Furthermore, numerous comprehensive prospective or retrospective analysis of KRAS and NRAS codons 12, 13, 59, 61, 117, and 146 demonstrated that patients with these mutations did not receive clinical benefits from anti-EGFR therapies.3 This evidence concerns the gene KRAS and neoplasm.