We therefore hypothesized that this detection of Q61 site mutations in tumours with acquired resistance may reflect a selection for more potent mutations to overcome the inherent poor translation of KRAS. Indeed, by analysing three separate cohorts of metastatic CRC patients with acquired resistance to anti-EGFR therapy27,28,29,30, we found that in all three groups, and in one combined subset of the groups, there was a significant enrichment in the number of KRASQ61 site mutations in comparison to a treatment naive background population (Table 1). The gene discussed is EGFR; the disease is colorectal carcinoma.