Moreover, these target genes have been proven to be down-regulated when WT1 is absent, resulting in abnormal expression of protein molecules, such as nephrin, podocin, a-actinin 4, and CD2AP, that maintain the stable structure of the podocyte slit diaphragm, which impairs the stability of podocyte actin, thereby being involved in the development of glomerulosclerosis. This evidence concerns the gene NPHS1 and glomerulosclerosis.