Mitochondrial deoxyribonucleic acid (DNA) damage, reduced adenosine triphosphate (ATP) production, and impaired mitochondrial biogenesis, marked by downregulation of regulators such as peroxisome proliferator-activated receptor-gamma coactivator (PGC)-1α, nuclear respiratory factor-1 (NRF1), and mitochondrial transcription factor A (TFAM), further compromise cellular bioenergetics, thereby exacerbating follicular arrest and ovulatory dysfunction in PCOS [18]. The gene discussed is TFAM; the disease is polycystic ovary syndrome.