Given that the USP6 gene locus is located on a breakage-prone region within chromosome 17, USP6 likely evolved through genomic translocation events resulting in the fusion of TBC1D3 and USP32. Given that mutations in NMDAR subunits, such as GluN1 and GluN2B, have been previously linked to intellectual impairment [15,16], it appears reasonable that hominoid-derived factors may have evolved to enhance downstream effectors associated with synaptic function and cognition/memory. The gene discussed is GRIN2B; the disease is Cognitive impairment.