A genomic study led by Pokorna, Orlickova, Machackova and colleagues reconstructed evolutionary trajectories in high‑grade serous ovarian cancer (HGSOC) beyond canonical BRCA alterations. By integrating whole-genome and longitudinal samples, the team charted clonal expansions, emergence of structural variants, and common routes to platinum resistance. The paper identifies recurrent genomic events that recur across patients and proposes timelines for when resistance-associated clones emerge during therapy. Authors highlight non‑BRCA mechanisms—such as copy-number changes and structural rearrangements—that shape disease evolution and treatment failure. For drug developers and trialists, the findings emphasize the need for longitudinal sampling and adaptive strategies to intercept evolutionary escape and for biomarker panels that extend past BRCA status.