SCN2A and epilepsy: Considering the various mutations and the consequent phenotypic spectra, it is now recognized that SCN2A gain of (increased or accelerated but not toxic) function mutations lead to early infantile-onset severe EEs such as Ohtahara syndrome, while loss-of-function mutations cause ASD, ID, or SCZ with later-onset, milder or even without epilepsies [24–26].