TP53 is the most frequently mutated tumor suppressor gene in cancers, and its wild-type form can inhibit tumor growth through multiple mechanisms (72).In the context of cisplatin resistance, TP53 mutations exert dual regulatory effects: on one hand, TP53 mutations can promote resistance phenotypes in mediastinal germ cell tumors (73)and high-grade serous ovarian cancer (74), patients harboring functional TP53 mutations exhibit the lowest cisplatin sensitivity and the poorest platinum-free survival prognosis (75). This evidence concerns the gene TP53 and ovarian serous adenocarcinoma.