Additionally, we show that among disease-associated GRIN2A variants, the DD/ID mutations localized within the linker/TMD region of GluN2A resulted in either a severe LoF (no current) or GoF (enhanced glutamate potency) consistent with prior characterizations of mutations from this regions20,22–25,28,34, while SCZ/epilepsy-linked missense mutations in the LBD displayed either no effect or partial LoF (reduced current or glutamate potency). Here, GRIN2A is linked to epilepsy.