Similarly, comprehensive genomic sequencing studies in high‐grade serous ovarian and prostate cancers have elucidated key resistance mechanisms—including BRCA1/2 reversion mutations and MDR1 overexpression in ovarian cancer, as well as a long tail of statistically significant mutations in prostate cancer—underscoring the utility of large‐scale genomic profiling in uncovering therapeutic vulnerabilities and enhancing my understanding of tumor evolution [14, 15]. This evidence concerns the gene BRCA1 and Familial prostate cancer.