In 80%–90% of colorectal tumours, tumourigenesis appears to be initiated following the loss of activity of the tumour suppressor gene APC via two inactivating mutations or one mutation followed by a loss-of-heterozygosity event.4 A member of the β-catenin destruction complex, loss of functional APC results in aberrant nuclear localisation of β-catenin, and dysregulated WNT signalling. Here, APC is linked to colorectal neoplasm.