KRAS and colorectal carcinoma: In this sense, CRC lesions may arise through acquisition of different molecular alterations; activation of oncogenes which differ from those included in KRAS-depending pathways, as well as inactivation of specific tumor suppressor genes (such as APC, p16, p53 and DCC) (12,13) or impairment of mismatch repair genes (including MLH1, MSH2 and, to a lesser extent, PMS2 and hMSH6) in the subset of CRCs associated with microsatellite instability (14).