Interesting, they showed that Wnt pathway abnormalities including the mutations of APC or CTNNB1 (coding β-catenin) were also found in 6 other SAs from non-FAP patients, suggesting that the pathogenesis of a subset of SAs may be involved in APC and other Wnt pathway abnormalities. This evidence concerns the gene CTNNB1 and Familial adenomatous polyposis.