EGFR ligands, such as TGFα, are often overexpressed in CRC and are thought to contribute to autocrine stimulation of tumour growth and invasiveness.3 Mutations in KRAS, which abrogate its GTPase activity and thus result in the constitutive activation EGFR signalling, are found in up to 45% of CRCs.4 More than 90% of the mutations in KRAS in CRC patients occur at just three positions: codons 12, 13 and 61. Here, EGFR is linked to neoplasm.