In addition, Gu et al. reported that administration of ApoA-I before the onset of reperfusion of myocardial infarction decreased creatine kinase release, diminished the production of TNF-alpha and IL-6 in cardiac tissue, and suppressed the endothelial expression of ICAM-1 in addition to neutrophil adherence and migration [18]. The gene discussed is ICAM1; the disease is myocardial infarction.