Nitric oxide (NO) produced from L-arginine by endothelial nitric oxide synthase (eNOS) exerts multiple beneficial functions, such as vasorelaxation, anti-inflammation and anti-apoptosis, in the vasculature and thus plays a critical role in vascular homeostasis and disorders.1 Abnormally decreased eNOS expression and activity, leading to impairment of the NO/cGMP pathway, are considered major contributors to the pathogenesis of various human diseases associated with endothelial dysfunction, such as hypertension, atherosclerosis and preeclampsia.1, 2, 3. Here, NOS3 is linked to preeclampsia.