NMDARs can not only improve learning and memory via sustaining LTP, but also cause synaptic plasticity damage and excitotoxicity through excitatory amino acid toxicity induced by NMDARs, resulting in learning and memory impairment, which is associated with Ca2+ disorders mediated by NR2B subunit (Martel et al., 2009). The gene discussed is GRIN2B; the disease is memory impairment.