However, if as we postulate here, increased NKCC1 expression in the developing Bloc1s8sdy/sdy hippocampus is a compensatory mechanism for reduced GABAergic innervation, then bumetanide may be ineffective or have deleterious effects in Bloc1s8sdy/sdy and other neurodevelopmental genetic defects affecting GABA neurotransmission such as schizophrenia. Here, SLC12A2 is linked to schizophrenia.