Kir4.1 expression levels are reduced in a vast array of CNS pathologies (for review, see Nwaobi et al., 2016), and restoration of astrocyte Kir4.1 levels in the striatum of Huntington’s disease model mice enhanced neuronal suvival and ameliorated motor deficits (Tong et al., 2014), suggesting that impaired K+ buffering may contribute to both genetic and aquired neurological disease. The gene discussed is KCNJ10; the disease is Huntington disease.