Oncogenic Wnt/β-catenin signalling is best exemplified in colorectal cancers where activating mutations in β-catenin or loss of APC (Adenomatosis Polyposis Coli) function (a key destruction complex protein) results in high cytoplasmic and/or nuclear β-catenin [18], constitutive β-catenin-TCF/Lef activity and expression of canonical Wnt target genes, such as MYC and CCND1[15]. This evidence concerns the gene HNF4A and colorectal cancer.