In view of the differential roles of Smad2 and Smad3 in hepatic fibrosis, Uemura et al. verified that Smad3 is more implicated than Smad2 in the morphological and functional maturation of myofibroblasts by transfecting HSC with adenoviruses expressing wild-type and dominant-negative Smad2 or Smad3 [28], whereas recent study from Koo et al. indicated that endoplasmic reticulum (ER) stress in HSC promoted hepatic fibrosis by inducing overexpression of Smad2. This evidence concerns the gene SMAD3 and Hepatic fibrosis.