We also observed that NOX4, a validated target of miR-25 and a known inducer of oxidative stress37, 46, 47, was increased in MMC treated with HG and TGF-β (diabetic conditions) and in the glomeruli of diabetic mice (in vivo) relative to corresponding controls, suggesting that downregulation of miR-25 via inhibition of its processing may be a new mechanism by which NOX4 and ensuing oxidant stress in augmented in the pathogenesis of DN. This evidence concerns the gene TGFB1 and liver dysplastic nodule.