A new study shows that the shift in intracellular chloride concentration ([Cl−]i) that occurs in the early postnatal period of mammalian neuronal development may regulate GABAA receptor (GABAAR) subunit composition. In immature murine cerebellar granule cells, overexpression of K+–Cl− cotransporter (KCC2) — which promotes a low [Cl−]i — was associated with a shift in α3 to α1 GABAAR subunit expression and an increase in δ subunit levels. Conversely, KCC2 downregulation increased α3 and lowered δ subunit levels. Thus, the [Cl−]i may provide a GABA-independent means of tuning phasic and tonic inhibition, mediated by α- and δ-containing GABAARs, respectively.