Although further studies are required to determine whether SMP30 is a key protein that directly prevented liver fibrosis in the present study, the fact that Smad3 deficiency led to up-regulated SMP30 expression supports the speculation that SMP30 expression may play an opposing role to that of Smad3 during the induction of hepatic fibrosis through an unknown mechanism. This evidence concerns the gene SMAD3 and Hepatic fibrosis.