The diminished inhibitory tone provided by FSPV+ GABAergic inhibitory interneurons onto assemblies of pyramidal output neurons in DS, Alzheimer’s disease and, possibly, at least some presentations of ASD, among other neuropsychiatric disorders stimulated interest in selective activation of GluN2A-containing NMDA receptors via GluN2A-subtype selective positive allosteric modulators (PAMs) [12,15,16,67]. The gene discussed is GRIN2A; the disease is Dravet syndrome.