Cancer‐critical genes with a high mutation prevalence in CRC generally have a homogeneous mutation pattern across metastatic lesions from the same patient [18, 19], although treatment pressure may cause subclonal expansion, as illustrated by the emergence of resistant subclones with pre‐existing or acquired KRAS mutations during anti‐EGFR therapy [20, 21]. The gene discussed is KRAS; the disease is colorectal carcinoma.