In addition to this direct action, chronically elevated Ang II could promote the generation of vascular oxidative stress, synthesis of reactive oxygen species (ROS), and activation of NADPH oxidase, which further induced the activation of NF-κB and secretion of proinflammatory cytokines, chemokines, and fibrogenic factors, thus resulting in the occurrence of inflammation and fibrosis as well as acceleration of the development of DN [48]. This evidence concerns the gene FMO5 and liver dysplastic nodule.