The article explores the interplay between Wnt signaling, β-catenin, and cadherin-mediated cell adhesion during tissue differentiation and embryogenesis. Wnts, a family of secreted signaling proteins, play crucial roles in regulating gene expression and cell proliferation. The central player in Wnt signaling is β-catenin, which is also involved in the cadherin complex that controls cell-cell adhesion and migration. The review highlights how Wnt signaling stabilizes and accumulates β-catenin, leading to its nuclear translocation and transcriptional activation. In contrast, the cadherin-catenin complex can sequester β-catenin at the cell surface, preventing it from entering the nucleus and activating transcription. The balance between these processes is regulated by phosphorylation, which affects the stability and availability of β-catenin. Additionally, the article discusses the role of growth factor receptors and tyrosine kinases in modulating β-catenin signaling by altering cadherin expression and the cadherin-catenin complex. The review also examines the connections between Wnt signaling and cadherin-mediated adhesion in stem cell organization and cancer, emphasizing the importance of maintaining proper cell fate, adhesion, and migration.The article explores the interplay between Wnt signaling, β-catenin, and cadherin-mediated cell adhesion during tissue differentiation and embryogenesis. Wnts, a family of secreted signaling proteins, play crucial roles in regulating gene expression and cell proliferation. The central player in Wnt signaling is β-catenin, which is also involved in the cadherin complex that controls cell-cell adhesion and migration. The review highlights how Wnt signaling stabilizes and accumulates β-catenin, leading to its nuclear translocation and transcriptional activation. In contrast, the cadherin-catenin complex can sequester β-catenin at the cell surface, preventing it from entering the nucleus and activating transcription. The balance between these processes is regulated by phosphorylation, which affects the stability and availability of β-catenin. Additionally, the article discusses the role of growth factor receptors and tyrosine kinases in modulating β-catenin signaling by altering cadherin expression and the cadherin-catenin complex. The review also examines the connections between Wnt signaling and cadherin-mediated adhesion in stem cell organization and cancer, emphasizing the importance of maintaining proper cell fate, adhesion, and migration.