GRIN2A and epilepsy: Work by Mota Vieira et al. [21] and Yong et al. [22] aimed to functionally characterise the epilepsy- associated variant GluN2A-S1459G and identified S1459 as a CaMKIIα phosphorylation site controlled in a development and activity-dependent manner whose mutation impaired interactions with SNX27 and PSD95 as well as GluN2A surface expression when ectopically expressed in cultured neurons.