It is noteworthy that in most CRC cells, the aberrantly active WNT/β-catenin signaling is not attributed to upstream WNT signals, as observed in other human cancers, but rather caused by the constitutive activation of β-catenin owing to loss-of-function mutations in the APC gene, as seen in HCT-15 and LoVo cells [26,27] or gain-of-function mutations in the β-catenin-encoding CTNNB1 gene, as found in HCT 116 cells [28]. This evidence concerns the gene APC and colorectal carcinoma.