In a rat PCOS model, increasing OS-induced GCs autophagy through the PI3K/AKT/mTOR pathway can be ameliorated by treatment with metformin [60], while the increased production of reactive oxygen species (ROS), which causes OS, induced apoptosis in granulosa-lutein cells via activation of the AMPK/AKT/Nrf2 signaling pathway [117]. The gene discussed is AKT1; the disease is polycystic ovary syndrome.