Altered function and expression of Wnt/β-catenin signaling components that result in β-catenin stabilization, such as mutations of APC, Axin or β-catenin itself, are known to contribute to a wide range of cancers, particularly CRC.6,37–41 In the present study, we described the discovery of a novel β-carboline structure-type compound Z86 that interfered with Wnt/β-catenin pathway by overactivation of GSK3β, promoted β-catenin degradation and finally exhibited efficient cell growth inhibition in colon cancer cells both in vitro and in vivo. This evidence concerns the gene APC and colonic neoplasm.