Through the CIN pathway, genetic alterations are generated in tumor suppressor genes (such as adenomatous polyposis coli (APC), tumor protein 53 (TP53) and SMAD family member 4 (SMAD4)) and oncogenes (such as K-ras proto-oncogene, KRAS and phosphoinositide 3-kinase catalytic subunit-α (PI3KCA)), resulting in CRC development [5,6,7]. This evidence concerns the gene KRAS and colorectal carcinoma.