Previous studies have reported that the Apc/Wnt pathway is an attractive target for the treatment of CRC.3 The adenomatous polyposis coli (Apc) tumour suppressor is mutated in 80%–90% of human colorectal tumours.4 Apc, along with axin and glycogen synthase kinase 3b (GSK3b), assembles a protein complex that targets β‐catenin for degradation, which is regulated by Wnt signalling.5 This is the main mechanism of Apc mutation leading to tumorigenesis, as the resulting increased availability of β‐catenin causes changes in the transcriptional process to decrease the amount of cell differentiation.6 This evidence concerns the gene APC and neoplasm.