Given that aberrant activation of the Wnt/β-catenin pathway, and its downstream transcriptional networks, is a common initiating event in CRC, and results from stabilisation and nuclear accumulation of the transcriptional co-activator β-catenin, we interrogated tumours arising in villin-creERT2 Krasfl/G12D and villin-creERT2 Kras+/G12D mice for nuclear accumulation of β-catenin. The gene discussed is KRAS; the disease is colorectal carcinoma.