In Dravet syndrome, caused by loss of function of the sodium channel Scn1a/Nav1.1, epileptic seizures were classically attributed to decreased excitability of inhibitory neurons, but Nav1.1 loss of function can also increase excitability of excitatory neurons (Liu et al., 2013), in part through a compensatory increase in Scn8a/Nav1.6 and decrease of SK2 calcium‐activated potassium channels (Ritter‐Makinson et al., 2019). The gene discussed is SCN8A; the disease is encephalopathy, progressive, early-onset, with brain edema and/or leukoencephalopathy.