A toxic gain-of-function trinucleotide repeat expansion of CAG within the coding region of the IT15 gene for the protein huntingtin on chromosome 4 leads to an elongated stretch of glutamine and eventual cell death of medium-sized spiny neurons (MSNs) in the striatum and cortex. The death of these MSNs that utilize GABA for neurotransmission leads to a lack of inhibition in basal ganglia circuitry. The disease manifests as chorea, cognitive disturbances, mood disorders, dystonia, rigidity, tics, myoclonus, and more. Here, HTT is linked to mood disorder.