Apc is implicated in the Wnt signaling pathway that is involved both in development and tumorigenesis. Human germline mutations in APC cause FAP [4,5], which is characterized by hundreds of adenomatous colorectal polyps, with an almost inevitable progression to colorectal cancer in the third and fourth decades of life. The phenotypical features of FAP and its variant, Gardner's syndrome, can be very variable. As well as colorectal polyps, these individuals can develop extracolonic symptoms, among which are upper gastrointestinal tract polyps, congenital hypertrophy of the retinal pigment epithelium, desmoid tumors, disorders of the maxillary and skeletal bones, and dental abnormalities [6]. While the heterozygous knockout mice for Apc develop adenomatous polyps predominantly in small intestine, the homozygous embryos die before gastrulation. To gain more insights into the effects of Apc loss in tissues other than gastrointestinal tract during life of animals and to circumvent the embryonic lethality associated with Apc nullizygosity, we created a mouse strain carrying a conditional allele of Apc (ApcCKO) in which exon 14 of the Apc is flanked by loxP sequences. The homozygous mice for the conditional allele are viable and indistinguishable to the normal mice, allowing us to study the roles of Apc in a tissue- and temporal-specific manner.