The role of PPAR‐γ in podocytes has been well studied.[15, 37] Podocyte‐specific PPAR‐γ knockout mice developed a more severe glomerulonephritis compared to wild‐type mice.[38] PPAR‐γ agonist, pioglitazone significantly decreased puromycin induced podocyte apoptosis and necrosis.[39] From another point of view, we reported a novel coactivator, NCOA3 of PPAR‐γ in this study. This evidence concerns the gene NCOA3 and glomerulonephritis.