It has been demonstrated that XO in the heart is activated by tumor necrosis factor (TNF)-α, which is upregulated after ischemia/reperfusion, and administration of anti-TNF-α antibodies at the onset of reperfusion partially restores nitric oxide- (NO-) mediated coronary arteriolar dilation and reduces superoxide production [55, 56]. The gene discussed is TNF; the disease is ischemia.