Additional pathways contribute to OC inflammation and immunosuppression: The PI3K/Akt/mTOR pathway is activated by inflammatory signals and drives M2 polarization, T cell exhaustion, and chemotherapy resistance (41–43)Wnt/β-catenin and MAPK/ERK signaling promote tumor proliferation, invasion, and immune evasion (44), while Notch signaling facilitates NLRP3 activation and Treg differentiation (45, 46). Here, AKT1 is linked to neoplasm.