Contrary to SCN1A loss-of-function mutations in patients with severe epilepsies such as Dravet syndrome22,34, SCN2A gain-of-function (increased or accelerated, but not toxic) has recently been recognized as a cause of early infantile-onset severe epileptic encephalopathies such as Ohtahara syndrome, whereas loss-of-function SCN2A mutations underlie ASD or intellectual disability with later-onset mild epilepsy or without epilepsy22,35,36. This evidence concerns the gene SCN2A and Epileptic encephalopathy.