The renoprotective action of an AT1R blocker (ARB) is strongly related to its ROS-lowering effects.10 In DN, the generation of ROS, AGT, and Ang II seems to increase remarkably when the vicious cycle of HG-ROS-AGT-Ang II-AT1R-ROS is activated.1–9. The gene discussed is AGT; the disease is liver dysplastic nodule.