This study showed that SH significantly suppressed the mRNA level and the protein expression of TGF-β1 and pSmad2/3 in BLM mice, implying that SH, through down-regulation of TGFβ1-Smad2/3 signal transduction, could at least partly alleviate BLM-induced formation and proliferation of myofibroblast. The gene discussed is SMAD2; the disease is Bloom syndrome.