The link of TSP-1 and TGF-β activation in several experimental kidney disease models [22], [23], [25], [32]-[34] as well as the fact of de novo upregulation of TSP-1 as an early response gene at sites of injury during experimental and human kidney disease [35], [36] suggests TSP-1 as a better and more specific anti-fibrotic target for kidney disease compared to overall blockade of TGF-β, since TGF-β activation not mediated via TSP-1 will not be affected. This evidence concerns the gene TGFB1 and kidney disorder.