Ctnnb1, encoding β -catenin, is a key gene in the Wnt/β -catenin signaling pathway. This pathway is pivotal in organ development, tissue homeostasis, and is often dysregulated in cancer [2]. β -catenin is involved in cell-cell adhesion and acts as a transcriptional co-activator, regulating the expression of target genes related to cell cycle regulation [1]. Genetic models, such as knockout (KO) or conditional knockout (CKO) mouse models, are valuable for studying its functions.

Knockout of the ieCtnnb1 enhancer, which is crucial for Ctnnb1 transcription in the intestine, led to a reduction in Ctnnb1 transcription. This compromised the canonical Wnt signaling in intestinal crypts, altered epithelial compositions, and hampered epithelial turnovers in normal conditions. However, it also prevented the occurrence and progression of Wnt/β -catenin-driven colorectal cancers, unveiling an enhancer-dependent mechanism controlling Wnt signaling dosage and intestinal epithelial homeostasis [2].

In conclusion, Ctnnb1 is essential for maintaining normal biological functions through its role in the Wnt/β -catenin signaling pathway. Studies using KO/CKO mouse models, like the ieCtnnb1 knockout, have revealed its significance in intestinal homeostasis and cancer development, providing insights into the mechanisms underlying these processes and potential therapeutic targets for related diseases [2].