Because of rather late onset of epilepsies in patients with SCN2A loss-of-function mutations and the reproduction of absence seizures in mice with dorsal-telencephalic excitatory neuron-specific Scn2a deletion, it would be now of interest whether the seizures are caused by Nav1.2 deficiency at the distal axons of neocortical or other dorsal-telencephalic excitatory neurons. Here, SCN2A is linked to epilepsy.