In addition, there is a kind of pathophysiological cross talk between the eNOS inhibitor ADMA and MPO, in which ADMA activates neutrophils and the release of MPO that in turn suppresses DDAH (enzyme for breakdown of ADMA) and leads to endothelial dysfunction (von Leitner et al, 2011). The gene discussed is NOS3; the disease is endothelial dysfunction.