An analysis of type IV collagen α3 chain-deficient mice, the model of human Alport syndrome, revealed that RAG1 deficiency in mice significantly ameliorated tubulointerstitial injury without amelioration in glomerular basement membrane (GBM) structures (LeBleu et al., 2008), but streptozotocin (STZ)-induced diabetic animal models using the same RAG1-deficient mice displayed no alteration in tubular injury when compared to control diabetic mice, even though RAG1-deficient diabetic mice exhibited low levels of albuminuria (Lim et al., 2010). The gene discussed is RAG1; the disease is Alport syndrome.