Examples include (i) miR-29b mimics, which interfere with Sp1-dependent, TGF-β/Smad3-mediated renal fibrosis, NF-κB–driven renal inflammation, and Th1-associated immune injury [191,192]; and (ii) inhibitors of miR-21 and miR-192, which reduce albuminuria and renal fibrosis, maintaining the structural and functional integrity of the kidney [193,194]. The gene discussed is SMAD3; the disease is renal fibrosis.