Alternatively, extrasynaptic GluN2B-NMDARs in HD models may destabilize synaptic AMPAR by sequestering CaMKII at extrasynaptic sites, preventing it from translocating to synapses to immobilize AMPARs due to the higher binding affinity of GluN2B for CaMKII compared to synaptic GluN2A-containing NMDARs [108]. This evidence concerns the gene CAMK2G and Huntington disease.