Platinum chemotherapy triggers cellular senescence in ovarian and lung cancer cells, paradoxically promoting malignancy through TGFβ ligand secretion. González-Gualda, Reinius and colleagues identified this senescence-associated secretory phenotype as a key driver of treatment resistance, revealing how damaged cancer cells can enhance tumor progression even as they stop dividing. This mechanism represents a significant advancement in understanding why platinum-based treatments often lose effectiveness over time. The finding suggests that combining traditional chemotherapy with senolytic agents—drugs that selectively eliminate senescent cells—could prevent or reverse resistance. Previous research has shown senescent cells accumulate with age and contribute to numerous pathologies, but this work directly links therapy-induced senescence to cancer progression. The therapeutic implication is profound: rather than viewing senescence purely as a tumor suppressor mechanism, oncologists may need to actively clear senescent cells during treatment. Clinical trials testing senolytics alongside chemotherapy are already underway for other cancers, and this research provides strong mechanistic rationale for their expansion to ovarian and lung cancers. The TGFβ pathway offers additional targetable nodes, potentially through existing inhibitors already in development.