Our findings showing that Ctnnb1 transcripts are up-regulated in Apc-mutant mouse colon epithelium as well as in Apc-mutant mouse OEAs, together with our findings that Ctnnb1 hemizygous gene dosage inhibited Apc mutation-dependent Ctnnb1 transcript induction in colon and ovarian tumor models imply that the Ctnnb1 gene is subject to feed-forward activation by β-catenin levels and β-catenin/TCF-regulated transcription. This evidence concerns the gene APC and ovarian neoplasm.