Among several candidates, we show that depletion of kallikrein−8 (Klk8) inhibits furin-independent hemicleavage in vitro as well as the Activin-A-induced tumor growth advantage in vivo, and that a point mutation in the furin motif of proActivin-A that blocks hemicleavage by recombinant KLK8 has a similar protective effect. The gene discussed is KLK8; the disease is neoplasm.