In the present study, we provided evidence that DMY attenuated TNF-α-induced endothelial dysfunction through downregulation of miR-21 expression, resulting in an increased expression and activity of DDAH1, which in turn leads to decreasing both intracellular and extracellular ADMA levels and enhancing eNOS (ser1177) phosphorylation and NO production. The gene discussed is NOS3; the disease is endothelial dysfunction.