Prospective follicular studies indicate that oxidative stress-induced telomere/DDR phenotypes and premature somatic follicular ageing are associated with shorter telomeres in PCOS granulosa and cumulus cells, as well as dysregulation of shelterin components (TRF1 localisation in cumulus cells; altered TRF2 expression in both cumulus and granulosa cells) and the upregulation of pro-apoptotic signalling (BAX) [66]. The gene discussed is BAX; the disease is polycystic ovary syndrome.