Ang II is emerging as a critical mediator of podocyte injury in diabetic kidney disease and has been shown to cause the rearrangement of cortical F-actin, redistribution of ZO-1, reduced α-actinin-4, dephosphorylation of nephrin, expression of focal adhesion kinase and a migratory phenotype switch in cultured mouse podocytes (20,21). This evidence concerns the gene TJP1 and diabetic kidney disease.