One of the most fundamental aspects of CRC tumorigenesis is the accumulation of mutations (e.g., mutant APC, KRAS, BRAF, and TP53) and epigenetic alternations (e.g., aberrant DNA methylation of MLH1) that mediate the initiation and formation of CRC (Grady & Pritchard, 2014; Okugawa, Grady, & Goel, 2015). This evidence concerns the gene KRAS and colorectal carcinoma.