These comprise focal amplifications, aneuploidy or loss of heterozygosity, for instance in tumour suppressors like APC and TP53. The impact of CNVs on therapy resistance has already been proven; for instance, CRC patients with amplifications in KRAS, ERBB2, MET and FGFR1 show poor prognosis and resistance to anti-EGFR therapy14, 15. The gene discussed is KRAS; the disease is colorectal carcinoma.