This makes alternative hits leading to WNT activation (including APC mutations) unlikely, given the findings of Crago and colleagues in desmoid-type fibromatosis in which CTNNB1 mutated and wild type cases were indiscernible in unsupervised clustering of U133A-derived gene expression profiles; in their analysis, the CTNNB1 wild type group of desmoid-type fibromatoses was shown to comprise cases with APC losses [20]. The gene discussed is APC; the disease is desmoid tumor.