Because the aforementioned association of a primary tumor site with cetuximab treatment was also noted in an expanded RAS wild-type population, primary expanded KRAS (exon 2, 3, 4) or NRAS (exon 2, 3, 4) mutations may not explain the different clinical benefits of cetuximab treatment in patients with different primary tumor sites. The gene discussed is KRAS; the disease is neoplasm.