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Compelling evidences from transgenic mice, immuno-precipitation data, gene expression analysis, and func-tional heterologous expression studies supported the role of Kv channel interacting proteins (KChIPs) as modulators of Kv4 (Shai) channels underlying the cardiac transient outward current and neuronal A-type current. Till now, there are four members (KChIP1-4)identified in this family. KChIPI is expressed predomi-nantly in brain, with relative abundance in Purkinje cells of cerebellum, the reticular thalamic nuclei, the medial habenular nuclei, the hippocampus, and stria-tu. Our results from in situ hybridization and immu-nostaining assay revealed that KChlP1 was expressed in a subpopulation of parvalbumin-positive neurons suggesting its functional relationship with the GABAergic inhibitory neurons. Moreover, results obtained from KChIPl-deficient mice showed that KChIPI mutation did not impair survival or alter the overall brain architecture, arguing against its essential function in brain development. However, the mice bearing KChIPl deletion showed increased suscepti-bility to anti-GABAergic convulsive drug pentylenete-trazole-induced seizure, indicating that KChIPl might play pivotal roles in the GABAergic inhibitory system.