AKT1 and polycystic ovary syndrome: Previous studies have expounded that Guizhi Fuling Wan represses GC autophagy in PCOS rats through enhancing the PI3K-Akt-mTOR pathway [36], and MT limits dehydroepiandrosterone-exposed KGN cell autophagy and apoptosis through activating the PI3K-Akt pathway and thereby mitigates PCOS [58], further supporting that the inactivation of the PI3K-Akt-mTOR pathway averted the effects of MT on SS-induced KGN cell autophagy.