Oocytes obtained during in vitro fertilization (IVF) cycles ideally are arrested in metaphase II (MII), which are characterized by the presence of a single polar body. They remain in arrest until after fertilization when time meiosis is resumed in a calcium-dependent manner. We present a case of a 23 year old gravida 0 with polycystic ovarian syndrome who presented for evaluation at our center after previously having failed two IVF cycles elsewhere. The patient subsequently underwent three controlled ovarian hyperstimulation cycles with either an antagonist or low dose luteal lupron down-regulation protocol. Vaginal oocyte retrieval (VOR) was performed 36 hours after administration of gonadotropin releasing hormone agonist (GnRHa) or human chorionic gonadotropin trigger. Cycle outcomes are demonstrated in Figure 1 . Oocytes were fertilized by intracytoplasmic sperm injection (ICSI) according to standard laboratory protocol. Embryos were cultured until day 7 of development. A substantial proportion of oocytes were noted to have one pronucleus (1PN) and two polar bodies (PB) at the time that the cumulus complex was denuded prior to ICSI ( Figure 2 ). The parthenogenetic oocytes were re-examined on the morning following VOR and were noted to have undergone cell division, with many that appeared similarly to cleavage stage embryos. In each cycle, there was complete embryo arrest prior to the blastocyst stage and no embryos were available for transfer. This case of recurrent parthenogenesis, accelerated cell division and complete developmental arrest highlights what potentially could be a rare genetic contribution to a cell-cycle regulatory deficiency. It has been suggested that defects in the c-mos/mitogen-activated protein kinase (MAPK) pathway in oocytes exhibit failure to arrest and premature activation ( 1 ). EMI2 is an additional regulatory factor that has been implicated in maintenance of arrest ( 2 ). It is unclear whether there is a failure of MII arrest due to functional deficiencies of MAPK and EMI2 or if there is an unidentified stimulus for escape which overrides these checkpoints. Attempts at fertilization of prematurely activated 1PNs have previously failed ( 3 ). Enhanced understanding of cell-cycle regulatory measures in oocytes and human preimplantation embryos may yield insight regarding diagnostic and therapeutic modalities for similar rare cases of spontaneous parthenogenesis.