In view of recent evidence for potential implication of herpes type viruses in the development of AD [84], it is worthwhile to mention that KDM1A inhibitors can block herpes virus lytic replication, reactivation from latency in vitro, as well as infection, shedding and recurrence in animal models [85–87], although ORY-2001 has not been evaluated in this context. The gene discussed is KDM1A; the disease is Alzheimer disease.