To further investigate podocyte injury, we isolated glomeruli from all experimental groups (Supplementary Fig. 3b) and found that podocyte-specific Fgf4 deficiency led to increased podocyte apoptosis, the accumulation of reactive oxygen species (ROS), and greater loss of podocytes in DKD mice (Fig. 2i). This evidence concerns the gene FGF4 and diabetic kidney disease.