As previously explained, numerous reports have shown that certain phosphorylations in tyrosine residues in the GluN2B subunit of NMDARs are strongly associated with their expression on the surface and that this balance in the phosphorylation state of the NMDARs and therefore of its location at the neuron level is altered after the induction of brain trauma [23] (Figure 8C,D). The gene discussed is GRIN2B; the disease is brain injury.