By integrating transcriptomics, network pharmacology, molecular docking and a clinically relevant orthotopic model, we here define: the optimal concentration window for GA+cisplatin synergy; the CXCL12/CXCR4–PI3K/AKT/mTOR pathway as a mechanistic hub; and prolonged survival without organ toxicity, thereby addressing the therapeutic void left by previous GA-ovarian cancer studies. This evidence concerns the gene AKT1 and ovarian carcinoma.