While low dose TNFα improved the systolic function of the heart, the higher doses of this cytokine suppressed myocardial contractility and increased myoglobin leak from an ex vivo model of functioning heart following ischemia.8 We have also shown that TNFα is an important inflammatory cytokine, which is released in response to myocardial ischemia in human models.9 In this study the dose-response effects of the E. Coli endotoxin lipopolysaccharide (LPS) on ischemic hearts during reperfusion has been assessed. The gene discussed is TNF; the disease is ischemia.