These results demonstrated that RhoA-Rock signaling positively regulated the wound closure induced by activin B. BrdU incorporation experiments further illustrated that compared with activin B group, activation of RhoA by RhoA L63-based lentivirus infection drastically increased the proliferation of epithelium keratinocytes on day 3 (Fig. 5A–C), and hair follicle cells on day 3 and 5 (Fig. 5B, C) during wound healing, whereas infection of dominant negative RhoA (N19) reduced epithelium keratinocytes and hair follicle cells proliferation both on day 3 and day 5 induced by activin B (Fig. 5). This evidence concerns the gene RHOA and lentivirus infection.