Hyperactivated Wnt signalling in CRC can also arise from mutations to AXIN2 [158] or CTNNB1 (β-catenin) [85], but account for a small percentage of cases in comparison to APC. While the kinetics by which APC is mutated differs between FAP and sporadic CRC patients, tumour cells with truncating APC mutations that maintain a ‘just-right’ level of Wnt signalling are positively selected for optimal tumour growth [159]. The gene discussed is APC; the disease is neoplasm.