Rather, the mRNA level for the β-catenin activity reporters that were elevated with APC truncating mutation was either unchanged or decreased in patients with CTNNB1 mutations when compared to patients with wild-type CTNNB1. Over 70% of the colorectal cancer patient samples with wild-type CTNNB1 displayed truncating APC mutations and another 9% displayed mutations in one or more other genes involved in β-catenin destruction (Axin1, Axin2, RNF43, and ZNRF3). This evidence concerns the gene APC and colorectal cancer.