Podocyte impairment has been shown to be involved in the development of proteinuria and the early pathological processes of diabetic kidney disease (DKD).[1,2] Recent studies indicate that the abnormal expression and distribution of podocyte surface marker proteins (such as nephrin and podocin), the reduction of podocytes, the loss of foot process fusion and other pathological changes may induce DKD and promote the disease progression.[3,4]. This evidence concerns the gene NPHS1 and diabetic kidney disease.