Nox2 and Nox5 were upregulated in Ang II treated podocytes.165 Consistently, Ang II receptor blockers inhibited Nox2 expression and were accompanied by increased SOD expression, decreased OS, and reduced renal and cardiac fibrosis.177 Specific overexpression of human Nox5 in vascular smooth muscle cells or mesangial cells led to glomerulosclerosis, inflammation, and renal fibrosis in diabetic mice.178. The gene discussed is CYBB; the disease is glomerulosclerosis.