The knock-down of NaV1.6 in the brain was shown to compensate the NaV1.1-gene mutation-induced imbalance of excitation over inhibition involved in epileptogenic disorders, which motivates the necessity to find specific NaV1.6 inhibitors to treat debilitating or fatal form of epilepsy such as the Dravet syndrome (Catterall, 2012; Anderson et al., 2017). Here, SCN8A is linked to encephalopathy, progressive, early-onset, with brain edema and/or leukoencephalopathy.