miR-21 was shown to suppress PTEN, a key modulator in DN [67]; miR-192 was shown to suppress ZEB2, which is responsible for controlling TGF-β-induced extracellular matrix proteins accumulating during DN [67], while miR-29c was shown to inhibit SPRY1, which involves albuminuria and kidney mesangial matrix accumulation in diabetic mice models [68]. The gene discussed is TGFB1; the disease is liver dysplastic nodule.