In the canonical pathway to CRC, the primary driving force is mutant APC-mediated activation of Wnt/b-catenin signaling 8, and the “just-right” level of Wnt/b-catenin signaling optimal for tumor formation is achieved mainly by the selection for specific APC mutant proteins based on their residual b-catenin-downregulating activity 9–12. Here, APC is linked to neoplasm.