The incorporation of the separated influence of the GluN2A-NMDAR and GluN2B-NMDAR functioning makes the model a candidate to explore learning in the diseased brain, as the Glu2NB-NMDAR normal functioning is crucial for healthy CA3-CA1 synapses, and its dysfunction is observed in cognitive deficits in neurological diseases (Kocsis, 2012; Pousinha et al., 2017, 2019; Adell, 2020). The gene discussed is GRIN2A; the disease is nervous system disorder.