Oxidative stress induces thiol oxidation in endothelial nitric oxide synthase (eNOS), which results in the attenuation of bioactive nitric oxide generation through Akt/eNOS signalling.6–8 The attenuation of endothelial nitric oxide activity plays an important role in the pathogenesis of coronary vasospasm.9 In general, severely high levels of serum homocysteine (>100 μM), such as this case, have been reported to induce vascular damage.10 Therefore, the impairment of nitric oxide activity by homocysteine might be a background of the cardiac event in this case. The gene discussed is NOS3; the disease is coronary vasospasm.