The transition from healthy gut epitheliumto colorectal cancer(CRC) is a multistep process that requires the accumulation of sequentialmutations in cancer driver genes.1 In mostcases, tumor formation starts with an inactivating mutation in the APC gene, resulting in constitutive WNT pathway activationthat eventually leads to adenoma formation.2 Subsequent critical alterations include P53 pathway inactivationand EGFR-pathway activation through mutations in P53 and KRAS, respectively, further contributingto the progression of adenoma to invasive carcinoma.3,4. Here, KRAS is linked to colorectal carcinoma.