In fact, although the above genetic model would predict that every tumour cell within a colon cancer allegedly initiated by an APC or β-catenin mutation should invariably be earmarked by the hallmark of constitutive Wnt activation, namely nuclear β-catenin accumulation, this is only observed in a minority of cells usually located at the invasive front of the primary lesion [4] from where they detach and invade the surrounding stroma [5], [6]. This evidence concerns the gene APC and colonic neoplasm.