We found that inactivation of Ep3 in Mos/Mps impairs myocardial repair after acute ischaemia; in contrast, forced activation of Ep3-mediated signalling in Mos/Mps accelerates healing in mice after MI by increasing recruitment of reparative Mos/Mps and secretion of proangiogenic VEGF. The gene discussed is VEGFA; the disease is myocardial infarction.