In addition, APC mutations were identified in 5 women with MCST, 4 of whom showed clinical features of FAP [2, 4, 13, 14], which explained the strong nuclear immunostaining for β-catenin, although in the absence of β-catenin mutations, further indicating that the Wnt/β-catenin/APC pathway mediated the occurrence and development of MCST. This evidence concerns the gene APC and Familial adenomatous polyposis.