Activated platelet–derived CXCL14 shows prominent thromboinflammatory influence in triggering monocyte migration [4,5,15], while it also exerts an angiostatic effect on endothelial cells and counteracts the angiogenic response of vascular endothelial growth factor and CXCL12 [4], which may impair vascular regeneration or re-endothelialization after MI. This evidence concerns the gene CXCL14 and myocardial infarction.