Thymosin β4 (Tβ4) plays a role in fibrosis, inflammation, and in the reparative process of injured cells and tissues. Here, we discuss our preliminary work on the protective effect of Tβ4 on carbon tetrachloride (CCl(4) )-induced acute hepatotoxicity. Our studies thus far indicate that Tβ4 can prevent necrosis, inflammatory infiltration, and upregulation of α1(and 2) collagen, α-SMA, PDGF-β receptor, and fibronectin mRNA expression; in addition, Tβ4 can prevent downregulation of PPARγ and upregulation of MECP2 mRNA levels in acute liver injury. Our initial work therefore indicates that Tβ4 can prevent the alteration of markers of hepatic stellate cell transdifferentiation, which suggests that Tβ4 could maintain the quiescent phenotypic state of hepatic stellate cells in the rat livers by restoring PPARγ and downregulating MeCP2 expression levels. More specifically, these preliminary studies suggest that Tβ4 might be an effective anti-inflammatory and antifibrotic drug for the treatment of liver fibrogenesis.