In normal-weight PCOS women, therefore, an association between SC abdominal adipose AKR1C3-mediated T generation and circulating cortisol could repress AP-1 transcription to counterbalance enhanced developmentally programmed AP-1 activity during accelerated adipogenesis in this adipose depot [9, 11, 12, 35, 60]. Here, JUN is linked to polycystic ovary syndrome.