Clinical trials using recombinant VEGFA to stimulate angiogenesis in patients with chronic myocardial ischaemia did not result in significant improvements in myocardial perfusion63, a result potentially explained by HDAC-mediated inhibition of MEF2 factors in these ischaemic regions: ischaemia has been shown to induce HDAC activity in the mouse heart after MI64, and pharmacological HDAC inhibition after MI can promote neovascularization and cardiac repair65. The gene discussed is HDAC9; the disease is myocardial infarction.