APC and colorectal neoplasm: 13–15 Over 80% of colorectal tumours carry loss-of-function mutation in APC and approximately 5% carry activating mutation in β-catenin,16,17 which leads to the constitutive activation of the Wnt/β-catenin pathway and thus contributes to cancer development.18 However, recent studies have shown that Wnt3 silencing remarkably attenuated the activation of the Wnt/β-catenin pathway and proliferation of CRC cells with mutation in APC or β-catenin.19 These data indicate that Wnt ligands can further activate a mutated Wnt/β-catenin pathway in which signalling activity is constitutively active.