Interestingly, a study reported that a rapid increase in proBDNF following status epilepticus induced by pilocarpine may be in part due to decreasing its cleavage due to a decrease in tissue plasminogen activator and an increase in plasminogen activator inhibitor-1 (PAI-1), an inhibitor of extracellular and intracellular cleavage, and that proBDNF is initially enhanced in response to the acute phase of epileptogenesis (Thomas et al. 2016). The gene discussed is PLAT; the disease is status epilepticus.