We re-analysed the WES data internally and selected models based on (1) the presence of predicted deleterious truncating nonsense (*), frameshift (fs), splice, and/or clinically relevant [34] recurrent ATM mutations and had variant allele frequency (VAF) data available; (2) excluded models, where possible, with co-occurring mutations in other main DDR genes such as BRCA1 or BRCA2 which may have confounded the results (Appendix A, Figure A1c), and (3) robust in vivo tumour growth characteristics (Figure 1a). The gene discussed is ATM; the disease is neoplasm.