Hence, the dramatic phenotypic differences brought about by oncogenic activation of the KRAS gene in compound Apc1638N/+/KRASV12G mice results from its synergistic action in promoting canonical Wnt signalling, as shown by the increase in TOP-Flash reporter activity and in the number of tumour cells earmarked by nuclear β-catenin accumulation [14]. The gene discussed is KRAS; the disease is neoplasm.