For blood vessels to deliver oxygen to distant tissues, they must remain intact. When the vessel is injured, bleeding is stopped by clotting (coagulation) factors that form a thrombus (clot) of fibrin threads that trap platelet aggregates. The protease thrombin is essential for fibrin formation and platelet activation. Platelets become activated when thrombin binds to several protease-activated G protein-coupled receptors (PARs) expressed on their surface (1). One member of the PAR family, PAR1, is not expressed by mouse platelets—yet, mouse embryos lacking this receptor die of fatal bleeding. The question is why? Emerging evidence implicates the clotting system in the building and stabilization of new blood vessels (angiogenesis) during embryonic development. On page 1666 of this issue, Griffin et al. report that expression of PAR1 by endothelial cells rescues the fatal vessel fragility and bleeding of mouse embryos engineered to lack