There is growing evidence of acquired impairment of DDAH activity through heredity, which would explain why Finnish men with a functional MACE of the DDAH1 gene had elevated plasma levels of ADMA and, therefore, an approximate 50-fold increased risk of CAD and a fivefold increased prevalence of hypertension when compared with non-carrier men in the Kuopio Ischemic Heart Disease Risk Factor Study21. This evidence concerns the gene DDAH1 and coronary artery disorder.