Integrating these findings, we postulated that a balance of HRD and APOBEC signature contributions exists and can be discriminated—if not dictated—by mutations in BRCA1/2 (germline and somatic), TP53, PIK3CA, and CDH1. For each tumor, we combined APOBEC C > T and C > G contributions, and plotted them against that of HRD (Fig. 5a). Here, TP53 is linked to neoplasm.