Khakh and colleagues ascribed these findings to defects in astrocytic Kir 4.1 channel expression in HD mice6, while Levine and colleagues have highlighted the contribution of neuronal downregulation of Kir2.1, Kir2.3 and Kv2.1 to the hyperexcitability of MSNs23. The gene discussed is KCNJ2; the disease is Huntington disease.