Embryonic diapause is a period of developmental arrest in which the embryo is maintained in a dormant state for an extended period of time. Over 130 species of mammals undergo diapause but the molecular mechanisms that control it remain unknown. During diapause, the mink blastocyst maintains an almost complete arrest of the cell cycle and a greatly reduced metabolism, DNA and protein synthesis (1). Treating mink with prolactin during diapause results in precocious termination of diapause, whereas treatment with dopamine agonists prevents implantation. The first signs of reactivation of the mink blastocyst from diapause are increased DNA and protein synthesis on the third day after prolactin injection (d3 PRL), with the first expansion of the blastocyst occurring at day 4 PRL (1). However, prolactin cannot reactivate embryos in culture and it is unknown how prolactin acts at the uterine level to induce reactivation. Previous attempts to culture mink embryos in vitro have been relatively unsuccessful with no mono-culture system identified that is able to sustain growth (2-5). Here we show that culture of diapause mink blastocysts in feline optimised cat media 2 (FOCM2) maintained viability and growth for a minimum of 4 days with increases in cell number and significant increases in diameter. Furthermore, this is the first time that mink diapause blastocysts have been reported to reactivate spontaneously in culture. This suggests that in the mink, embryonic diapause is under uterine control as opposed to the absence of a critical factor that the blastocyst requires to reactivate.