Glomerulosclerosis firstly induces the thickening of the GBM (with an increased production and low clearance of GBM structural proteins), associated with podocyte detachment from the GBM (potentially followed by their apoptosis or their transformation into mesenchymal cells, which in turn promotes glomerulosclerosis)—mechanisms supported by high levels of TGF-β. This evidence concerns the gene TGFB1 and glomerulosclerosis.