Based on the notion that the inhibition of Smad2/3 phosphorylation will reduce fibrosis levels, we successfully identified the ability of MA to suppress Smad2/3 phosphorylation in vivo as well as in vitro, suggesting that negative regulation of MA in renal fibrosis occurs through the downregulation of p-Smad2/3, at least in part. Here, SMAD2 is linked to renal fibrosis.