Studies initially demonstrated that benefit derived from the addition of EGFR mAb has limited to patients with tumours wild-type (WT) at KRAS exon 2 and subsequently to “extended RAS” WT tumours, which do not harbour activating mutations at KRAS exons 2,3 and 4 or NRAS exons 2, 3 and 4 [4–6, 8, 10]. The gene discussed is NRAS; the disease is neoplasm.