Considering the strong relation between MPO and systemic endothelial function, as a readout of vascular NO bioavailability [23,24] on the one hand and the robust data showing a markedly diminished vascular NO availability in AMI on the other hand [25,26], it might also be speculated that systemic activation of leukocytes, particularly via secretion of MPO, is one mechanism by which AMI leads to systemic endothelial dysfunction. The gene discussed is MPO; the disease is endothelial dysfunction.