For instance, recent evidence in animal models suggests increasing the availability of NMDAR at the cell surface through Ephrin-B2 receptor activation in certain anti-NMDAR autoimmune encephalitis [73], while selective inhibition of GluN2A subunits [25] and microglia [78] would be more adequate in SLE patients bearing dsDNA/NMDAR antibodies. Here, GRIN2A is linked to systemic lupus erythematosus.