Therefore, our findings showing that Ctnnb1 hemizgyous state did not prevent development of Apc- and Pten-mutant OEAs even though there was a reduction in β-catenin levels and expression of some β-catenin/TCF-regulated genes suggest that retention of Myc induction in OEAs with hemizygous Ctnnb1 function, but not in Apc-deficient colon epithelium with hemizygous Ctnnb1 function, may be a contributing factor in the observed differences in tumor development in the two tissues. Here, CTNNB1 is linked to neoplasm.