The molecular basis of CRC involves in most cases the activation of the Wnt–β-catenin signaling pathway by the mutation of intracellular components such as APC, AXIN, and CTNNB1/β-catenin genes or the epigenetic alteration of Wnt inhibitors such as DKK-1, SFRPs, and WIF, considered the initial steps in colorectal tumorigenesis [2]. This evidence concerns the gene APC and colorectal carcinoma.