Inactivated mutations in the APC gene or activating mutations in the β-catenin-encoding gene CTNNB1 together account for the majority of genetic lesions in CRC cells, which lead to stabilization and ensuing nuclear translocation of β-catenin to facilitate TCF/LEF-dependent transcription of WNT/β-catenin signaling target genes to drive cell proliferation, metastasis, and cancer stemness [6,7,8]. Here, HNF4A is linked to colorectal carcinoma.