In 2010, following this major step and based on the observation that most patients with KRAS exon 2 wild-type tumours still did not respond to Cetuximab, further analysis proved that mutations in either KRAS (exons 2, 3 and 4) or the closely related NRAS (exons 2, 3 and 4) genes were associated with the lack of response to anti-EGFR treatment [9]. Here, EGFR is linked to neoplasm.