We have previously shown that blockade of KCa3.1 prevented the development of extracellular matrix deposition and fibrosis in diabetic nephropathy through inhibition of the TGF-β1/Smad signaling pathway [11], limiting activation of renal fibroblasts [20], suppression of TGF-β1 induced monocyte chemoattractant protein-1 (MCP-1) expression and high glucose induced chemokine (C-C motif) ligand 20 (CCL20) expression in renal proximal tubular cells [21, 22]. This evidence concerns the gene KCNN4 and diabetic kidney disease.