In colon cancer cells that express high levels of DACT1, we propose that DACT1 interacts with β-catenin, after which DACT1 binds to and inhibits GSK-3β, which results in the release of β-catenin from the destruction complex, increased intracellular β-catenin levels, and its subsequent accumulation in the nucleus. This evidence concerns the gene DACT1 and colonic neoplasm.