HK-2 cells were stimulated by TGF-β, a critical mediator of renal fibrosis (Fig. 6A), resulting in significant increases in the phosphorylation of Smad2/3 and expression of Smad 4, which are downstream signals of TGF-β, along with increased expression levels of α-SMA. This evidence concerns the gene ACTA1 and renal fibrosis.