It was shown that overexpression of Nox4 could reverse the improvements in cardiac function conferred by Tanshinone IIA in heart-failure rats: Nox4 overexpression negated Tanshinone IIA’s ability to reduce left ventricular type I and III collagen, TGF-β, α-smooth muscle actin (α-SMA), MMP2, and MMP9. The gene discussed is NOX4; the disease is heart failure.