WT1 and glomerulosclerosis: 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.