It was shown that some β-catenin-binding activity (and resulting β-catenin degradation) in one of the APC alleles was always retained, suggesting an optimal level of β-catenin/TCF-mediated transcription for tumour progression – as mutations that completely abolished the β-catenin-binding ability of APC were not selected for (Albuquerque et al., 2002). Here, APC is linked to neoplasm.