Because of our findings regarding the role of the Sirt1/Claudin-1 axis on podocyte function, many other reports have shown that depressed Sirt1 and amplified Claudin-1 were detectable in damaged podocytes in DN [10, 11] and in other kidney diseases such as focal segmental glomerulosclerosis [12, 13] and hypertension-induced glomerular sclerosis [14]. This evidence concerns the gene CLDN1 and focal segmental glomerulosclerosis.