A shift in the balance of synaptic to extrasynaptic NMDAR signaling contributes to HD pathology, as chronic extrasynaptic NMDAR blockade attenuates mHtt-induced striatal atrophy and motor learning deficits in YAC128 mice, transgenic mice that express the human huntingtin protein containing a 128 CAG repeat expansion [195, 196]. This evidence concerns the gene HTT and Huntington disease.