Notably, a well-described developmental switch from NR2A to NR2B subunit expression is considered a hallmark of synaptic maturation that promotes memory formation, and elevation in miR-142-5p (which would suppress NR2B expression) is associated with amyloid beta pathology in postmortem brain samples of subjects with Alzheimer’s disease (AD) [27]. The gene discussed is GRIN2A; the disease is Alzheimer disease.