As the activity of DDAH is reduced and the generation of ADMA increased via up-regulation of protein arginine methyltransferase 1 (PRMT1) in animal fibrillating atria4 also explaining the increased ADMA levels in human AF, it can be hypothesized that the alternative AGXT2-mediated elimination pathway of dimethylarginines could play an important role in the pathogenesis of AF. The gene discussed is PRMT1; the disease is atrial fibrillation.