This interplay also underpins disease pathogenesis: in PCOS, synergistic defects in phosphorylation (IRS-1), ubiquitination (AR), and acetylation (PDK4) drive hyperandrogenism and follicular arrest; in POI, coordinated abnormalities in SUMOylation, ubiquitination, and lactylation accelerate follicle depletion via meiotic dysfunction and metabolic disorders. The gene discussed is IRS1; the disease is polycystic ovary syndrome.