EZH2 and myocardial infarction: Moreover, we promisingly demonstrate that pharmacological Ezh2 inhibition, with GSK-343, reduced the H3K27me3 mark specifically at the promotor of bivalent genes (such as DLL1, VEGFA, IRF4) resulting in accelerated resolution of the inflammatory phase, reduced infarct scar expansion, and improved cardiac function post-MI in vivo.