In addition to affecting genes, oxidative stress can also promote the survival and proliferation of ovarian cancer cells by regulating signalling pathways such as the Kelch-like ECH-associated protein 1 (Keap1)–nuclear factor erythroid 2-related factor 2 (Nrf2)–antioxidant response element (ARE) signalling pathway, phosphatidylinositol-3-kinase (PI3K)–protein kinase B (AKT)–mammalian target of rapamycin (mTOR) signalling pathway, and the Wnt/β-catenin signalling pathway. This evidence concerns the gene AKT1 and ovarian cancer.