The heterozygous mutation is inherent in all cases of familial adenomatous polyposis.(13-15) The APC protein forms molecular complexes that are capable of eliminating the intra-cytoplasmic beta-catenin, inducing its degradation.(1,4,12) In the epithelium of the large intestine, APC expression is restricted to regions in which cell replication has ceased, and terminal differentiation was established.(13). This evidence concerns the gene CTNNB1 and Familial adenomatous polyposis.