KRAS and colorectal cancer: It is now widely accepted that sporadic colorectal cancers frequently arise from preneoplastic lesions through the activation of oncogenes (KRAS and BRAF) as well as the inactivation of tumour suppressor genes (APC, p16, p53, and DCC) and mismatch repair genes, such as MLH1 and MSH2 and, to a lower extent, PMS2 and hMSH6[1].