This study investigates the role of stabilized β-catenin in intestinal tumorigenesis in mice. The researchers constructed a mutant β-catenin allele by targeting exon 3, which encodes serine and threonine residues phosphorylated by glycogen synthase kinase 3β (GSK3β), with loxP sequences. When germline heterozygotes were crossed with mice expressing Cre recombinase in the intestines, exon 3 was deleted in the offspring intestines, leading to the formation of adenomatous intestinal polyps similar to those seen in ApcΔ716 knockout mice. Nascent microadenomas were also observed in the colon. These results provide experimental evidence that activation of the Wnt signaling pathway can cause intestinal and colonic tumors. The study highlights the importance of β-catenin in intestinal tumorigenesis and suggests that Wnt signaling plays a crucial role in this process.This study investigates the role of stabilized β-catenin in intestinal tumorigenesis in mice. The researchers constructed a mutant β-catenin allele by targeting exon 3, which encodes serine and threonine residues phosphorylated by glycogen synthase kinase 3β (GSK3β), with loxP sequences. When germline heterozygotes were crossed with mice expressing Cre recombinase in the intestines, exon 3 was deleted in the offspring intestines, leading to the formation of adenomatous intestinal polyps similar to those seen in ApcΔ716 knockout mice. Nascent microadenomas were also observed in the colon. These results provide experimental evidence that activation of the Wnt signaling pathway can cause intestinal and colonic tumors. The study highlights the importance of β-catenin in intestinal tumorigenesis and suggests that Wnt signaling plays a crucial role in this process.