This excess synaptic activity is driven in part by glioma-derived glutamate, which can cause down-regulation in surrounding neurons of the potassium chloride cotransporter (KCC2) that normally extrudes Cl– to maintain the GABA reversal potential (Campbell and others 2015); lowering KCC2 expression increases intracellular Cl–, in turn leading to a shift in neuronal GABAA receptor signaling from hyperpolarizing to depolarizing and thereby promoting peritumoral neuronal hyperexcitability (MacKenzie and others 2016). Here, SLC12A5 is linked to glioma.