GRIN2A mutations in EAS are spread across the gene and our work, combined with others where EAS- or early-onset epileptic encephalopathy associated GRIN2A mutations (studied generally in the homozygous state) have been shown to affect zinc sensitivity16, 26, increase glutamate potency27, 28, alter channel gating kinetics17, 28 or eliminate the Mg2+ block11, indicate a complex pathophysiological picture. Here, GRIN2A is linked to genetic developmental and epileptic encephalopathy.