Tumours from primed and control mice had similar mutation burdens (around 6 single-nucleotide variants (SNVs) per Mb), except for those arising on the Trp53null background that had had a significantly higher mutation burden (mean (s.d.): 9.9 (3.1) SNVs per Mb) and colonic, but not SI, tumours on the Trp53hetN1-ICDhet background had a significantly lower mutation burden (mean (s.d.): 4.0 (1.1) SNVs per Mb) (Supplementary Fig. 2), probably reflecting differential survival of transforming events that would be eliminated through p53-mediated apoptosis in WT mice. This evidence concerns the gene TP53 and neoplasm.