In addition, LPS activates the serum kinase c-Jun N-terminal kinase (JNK) and the inhibitor of nuclear factor-κB kinase (IKK) to induce insulin receptor substrate-1 (IRS-1) serine phosphorylation, leading to impairment of the insulin metabolic pathway and triggering IR (Saad et al., 2016; Guadagnini et al., 2019), and hyperinsulinemia may interfere with follicular development, leading to excessive androgen production by follicular theca cells of the ovary, which consequently leads to PCOS. The gene discussed is IRS1; the disease is polycystic ovary syndrome.