Consistent with this, Liu et al. demonstrated that repeated administration of (S)-ketamine for 7 consecutive days reversed CUMS-induced depression-like behaviors and synaptic ultrastructural alterations in the hippocampus of mice via the upregulation of GluN1 and GluR1 levels and downregulation of GluN2B levels (Liu et al., 2023), whereas there was no significant effect of CUMS or ketamine treatment on GluN2A subunit expression. The gene discussed is GRIN2A; the disease is depressive disorder.