It was shown that the pathophysiology of PCOS involves hormonal imbalance, metabolic dysfunction, and inflammation via the activation of nuclear factor kappa-light-chain-enhancer of activated B cells p65 subunit/IL-1β (NF-κB p65/IL-1β) and AMPK/PI3K/AKT, as well as the downregulation of nuclear factor erythroid 2–related factor 2 (Nrf2) and upregulation of the NLRP3 inflammasome [90,91]. This evidence concerns the gene AKT1 and polycystic ovary syndrome.