In one case (CRUK0587; adenosquamous carcinoma) we observed evidence of parallel subclonal inactivation of TP53—in addition to a clonal LOH event encompassing 17p, we observed a stopgain TP53 driver mutation (S34X) present in one of the primary regions while a distinct splice site driver mutation was observed in the metastatic samples (Extended Data Fig. 6f). No cancer genes harboured a significant enrichment for metastasis favoured mutations in either histological subtype. The gene discussed is TP53; the disease is cancer.