Meanwhile, our another proposal that the functional interaction of myoclonin1 and the transient receptor potential M2 channel (TRPM2) plays a role in the pathogenesis of JME19 may still survive as a possible pathomechanism of JME because of the TRPM2 expression in ependymal cells in addition to neurons. The gene discussed is TRPM2; the disease is juvenile myoclonic epilepsy.