The observed relative increase in the number of Apc1638N/+/KRASV12G tumour cells earmarked by nuclear β-catenin is of importance in view of the so-called “β-catenin paradox” [7]: notwithstanding the fact that loss of APC function is common to all tumour cells and is predicted to result in the intracellular and nuclear accumulation of β-catenin, this is only observed in a minority of cancer cells undergoing an epithelial-to-mesenchymal transition (EMT) and non-randomly distributed at the invasive front of the tumour mass [4], [5] (see also Fig. 2a). This evidence concerns the gene APC and neoplasm.