Therefore, we hypothesized that although the regulation of VEGF-A and CTGF induced by ELFPMF might partially aggravate the development of DN, ELFPMF might ameliorate kidney complications induced by diabetes through other mechanisms, because the pathogenesis of DN is complex and involves multiple pathways that lead to kidney injury, including the polyol pathway [30], protein kinase C [31], advanced glycation end products [32], high glucose-induced generation of reactive oxygen species (ROS) [33], and proinflammatory cytokines. This evidence concerns the gene CCN2 and liver dysplastic nodule.