It could furthermore be shown that there is an increase in E-selectin expression after myocardial infarction in vivo [132], and in the presence of E-selectin, an increased neutrophil infiltration in the infarcted area could be found, suggesting a role of E-selectin in binding of neutrophils to the activated/damaged endothelium and thereby the development of ischemia/reperfusion injuries [132]. This evidence concerns the gene SELE and myocardial infarction.