In agreement with this hypothesis, an excessive accumulation of Rph3A at the postsynaptic membrane, and an enhancement of Rph3A/GluN2A interactions and GluN2A synaptic levels, have been correlated with pathological synaptic plasticity and absence of synaptic depotentiation in models of late stage of Parkinson’s disease and drug-induced dyskinesia [16]. The gene discussed is GRIN2A; the disease is Parkinson disease.