APC and desmoid tumor: Interestingly, in most (80–90%) sporadic cases of desmoid-type fibromatosis, somatic mutations of adenomatous polyposis coli (APC) gene, as well as activating mutations in CTNNB1, the beta-catenin gene, usually result in the accumulation of beta-catenin which triggers fibroblastic proliferation through a nuclear mechanism [16].