The development of a broad range of CRCs can be explained by the multistep carcinogenesis model and high microsatellite instability (MSI-H) resulting from deficiencies of the mismatch repair (MMR) gene set, which consists of MSH2, MLH1, MSH6, and PMS2. The MSI-H phenotype is found in both hereditary non-polyposis colorectal cancer (HNPCC) with germline mutation in MMR gene set (3%) and sporadic CRCs with CpG island methylator phenotype in MMR gene set (12%), together which account for approximately 15% of all CRCs [1]. This evidence concerns the gene MRC1 and hereditary nonpolyposis colon cancer.