Whereas in the time the CAIRO2 trial was performed cetuximab was prescribed to unselected patients, regardless of tumor characteristics, it was shown shortly thereafter that patients carrying a somatic mutation in Kras codon 12 or 13 are resistant to treatment with cetuximab.[29–32] More recently, patients with mutations in Nras were also shown not to benefit from treatment with anti-epidermal growth factor antibodies.[33] More somatic mutations precluding EGFR inhibitor efficacy may be discovered. The gene discussed is KRAS; the disease is neoplasm.