SLC12A5 and epilepsy: It is critical to distinguish how intracellular chloride accumulation and increases in extracellular potassium contribute to GABAA-mediated excitation, since these levels are coupled through the primary chloride efflux mechanism, the potassium-chloride co-transporter, KCC2 [11], [7], [12], [5], which has been suggested as a potential therapeutic target to suppress pathological states in epilepsy and pain [13].