The mechanisms for inherent and acquired resistance to anti-EGFR monoclonal antibodies seem to overlap in CRC, as KRAS, NRAS and EGFR ectodomain mutations [the latter have also been detected in patients with SCCHN (76, 77)], and MET and KRAS amplification have also been detected in circulating tumor DNA in patients with acquired resistance to anti-EGFR antibodies (78–83). This evidence concerns the gene KRAS and neoplasm.