TGF-β1 over-expression in podocytes can activate p38 MAPK and caspase-3, induce podocyte apoptosis, and trigger EMT, ultimately give rise to proteinuria and glomerular sclerosis induced by podocyte detachment from the GBM when the cell phenotype is altered and cell structure and function is lost [17, 18]. Here, CASP3 is linked to glomerulosclerosis.