Despite intense investigation on apoptosis pathways, exactly how apoptosis is regulated in various primary cells remains understudied and continues to reveal unexpected mechanisms. While a strict regulation of apoptosis is critical for the long-term survival of postmitotic cells, mitotic cells need to maintain their ability to activate apoptosis rapidly, as they can be at continual risk of becoming cancerous.1 Therefore, cells must efficiently balance the need for having a primed apoptotic pathway vs. the risks associated with inadvertent cell death. This balance is particularly important during embryogenesis, where human embryonic stem (hES) cells proliferate rapidly and differentiate, leading to the development of an entire organism.2 While optimal hES cell survival is necessary for development, the ability of these cells to respond rapidly to DNA damage by apoptosis and maintain genomic integrity is also critical to prevent propagation of mutations in the developing embryo.3 Indeed, hES cells are known to be highly sensitive to DNA damage,4,5 and our recent results have uncovered a novel mechanism by which these cells are primed for rapid apoptosis.6