Our studies were unable to determine whether macrophages, podocytes, TECs or other cells are dominant in causing fibrosis in DN, but do suggest a prominent role of TLR4 activation in the process as has been demonstrated in models of hepatic fibrosis [23], cardiac fibrosis after myocardial infarction [36] and in kidney following ureteric obstruction [37], [42]. This evidence concerns the gene TLR4 and liver dysplastic nodule.