DNMT3A and infarction: Here, expression of HMGB2 and PLBD1, which act pro‐inflammatory in a paracrine fashion either by acting as cytokine itself of by generating lipid mediators of inflammation, respectively, and were both shown to correlate with cardiac functional deterioration post‐infarction,25, 46, 47 were specifically up‐regulated in LOY monocytes of patients simultaneously harbouring DNMT3A CHIP‐driver mutations.