This has led to compelling data that NMDAR mutations contribute to epilepsy with studies suggesting that GRIN2A mutations are associated with 9% of epilepsy-aphasia spectrum disorders and 20% of Landau-Kleffner Syndrome (LKS), continuous spikes and waves during slow-wave sleep (CSWS), and atypical rolandic epilepsy (aRE) cases [13–15,29,38]. The gene discussed is GRIN2A; the disease is developmental and/or epileptic encephalopathy with spike-wave activation in sleep.