Circulating ADMA is a marker of cardiovascular disease and mortality (Böger et al., 2009a), and mouse models in which DDAH – the major enzyme responsible for the metabolic degradation of ADMA – was genetically deleted show endothelial dysfunction and elevated systemic arterial pressure, while mice in which DDAH is overexpressed show decreased ADMA levels and protection from vascular damage (Leiper et al., 2007; Hu et al., 2011). This evidence concerns the gene DDAH2 and endothelial dysfunction.