For a long time, the development of CRC was thought to follow a molecularly well‐defined route with the inactivation of the adenomatous polyposis coli (APC) gene as the initiating event followed by the activation of the KRAS oncogene and the inactivation of TP53 as the tumor progresses to a metastatic carcinoma (Fearon & Vogelstein, 1990). This evidence concerns the gene KRAS and colorectal carcinoma.