Inappropriate perforin activity has also been implicated in a variety of pathologies, including cerebral malaria, insulin-dependent diabetes, juvenile idiopathic arthritis and postviral myocarditis9, 10, 11 as well as therapy-induced conditions such as allograft rejection and graft versus host disease.2, 12, 13 Since perforin is expressed exclusively by CTL and NK cells it is possible that a selective inhibitor of this protein could be used to treat autoimmune diseases or therapy-induced conditions characterised by dysfunction of this pathway. The gene discussed is PRF1; the disease is juvenile idiopathic arthritis.