The genetic basis of cancer was firmly established by the discovery and cloning of the adenomatous polyposis coli (APC) gene, whose loss of function is likely the most common cancer initiator in CRC.5–9 This was followed by the recognition that CRC carcinogenesis involves several genetic events and is a multistage process.10,11 Individuals that are born with a heterozygous APC deficiency develop familial polyposis (FAP), which, if left untreated, develops into colon cancer. Here, APC is linked to colonic neoplasm.