Intriguingly, mutations in GRIN2A, but not AKAP11, are associated with certain epilepsy disorders (including epilepsy-aphasia syndromes [1, 3] and severe developmental and epileptic encephalopathy [71]), and a drug that acts as a positive allosteric modulator of GRIN2A-containing NMDA receptors (GNE-0723) reduces spontaneous power (including slow oscillation power) in mouse models of Dravet syndrome and Alzheimer’s disease [35, 72]. This evidence concerns the gene GRIN2A and encephalopathy, progressive, early-onset, with brain edema and/or leukoencephalopathy.