Finally, the markedly increased risk of death (8-fold) of high AREG mRNA in KRAS mutant versus KRAS wild-type CRC patients in multivariate analysis could be explained if AREG is viewed as a protein regulated by KRAS-dependent transcription factors: the former group includes tumours bearing KRAS mutations with a markedly pro-survival, proliferative activating effect, whereas the latter group includes KRAS wild type tumours addicted to active EGFR signalling that is amenable to abrogation by cetuximab. The gene discussed is AREG; the disease is neoplasm.