PPARγ agonists (15d-PGJ2, troglitazone, and ciglitazone) can inhibit TGF-β/SMAD signaling pathways to alleviate renal fibroblast activation, resulting in decreased expression of connective tissue growth factor (CTGF) and extracellular matrix synthesis [47], all contributing to reduced renal fibrosis progression. The gene discussed is CCN2; the disease is renal fibrosis.