We recently identified the gene encoding the activin betaA chain as a novel injury-regulated gene. We showed that activin over-expression in the skin of transgenic mice enhances the speed of wound healing but also the scarring response. By contrast, inhibition of activin action by over-expression of the activin antagonist follistatin caused a severe delay in wound repair, but the quality of the healed wound was improved. In a search for activin-regulated genes in keratinocytes we identified the Mad1 transcription factor as a direct target of activin in these cells. Since Mad1 inhibits proliferation and induces differentiation of various cell types, our results suggest that activin regulates these processes in keratinocytes via induction of mad1. In addition to its role in the skin, we recently identified activin as a novel neuroprotective factor in vivo. Together with results from other laboratories, these findings suggest that activin is an important player in inflammation, repair and cytoprotection in various organs.