KLF15 and glomerulosclerosis: Previous studies indicated that podocyte-specific Klf15-KO mice in the unperturbed state did not develop significant proteinuria or glomerulosclerosis, but in Lipopolysaccharide (LPS) or Adriamycin (ADR)-induced proteinuric murine models, loss of KLF15 led to a significant increase in the susceptibility to podocyte injury, indicating a critical role for KLF15 as a regulator of podocyte differentiation protecting against podocyte injury 27 (Fig. 1).