Interestingly, the susceptibility to depolarization block and subsequent hypoexcitability in inhibitory interneurons reported here indicates that a mechanism for seizures in SCN8A DEE, a disorder characterized primarily by GOF sodium channel mutations, shares many similarities to that of Dravet syndrome, a disorder primarily characterized by sodium channel haploinsufficiency in inhibitory neurons. Here, SCN8A is linked to encephalopathy, progressive, early-onset, with brain edema and/or leukoencephalopathy.