In certain neuropathological states, impaired KCC2 function and/or enhanced NKCC1 function can lead to intracellular Cl− accumulation and GABA-mediated excitation (Ben-Ari et al., 2012); however, the potential role of impaired CCCs in the BG during early symptomatic HD is unknown. This evidence concerns the gene SLC12A5 and Huntington disease.