Proliferative disorders, as tumors, are central to a variety of pathological states involving oxidative stress. Among brain tumors, malignant gliomas are composed by two cell types: cancer stem cells (CSCs) and parental cells. Gliomas are very aggressive tumors because of CSCs brain infiltration efficiency. The Chloride Intracellular Channel 1 (CLIC1) is expressed in high grade gliomas. CLIC1 is a protein mainly localized in the cytoplasm that is able to translocate into membranes where it acts as a Cl^- channel. Our experiments aim to understand CLIC1 functional expression as a common mechanism of infiltration. We have isolated CSCs from two different human glioblastoma samples: CLIC1 is expressed in both cytoplamic and transmembrane isoforms. Given that CLIC1 is expressed in all neurosphere cells, we silenced it by RNA interference to unravel its function. We found that CLIC1 deficient cells (siCLIC1) migrated about 50% less efficiently than control cells (siRNA against luciferase, siLUC). Is this phenotype due to the absence of CLIC1 functional expression in plasmamembranes? To solve this task, we performed electrophysiological experiments: Cl^- currents mediated by CLIC1 were estimated by analytical subtraction after addition of a specific inhibitor (IAA94). The results showed that siCLIC1 cells did not display IAA94-sensitive currents, while siLUC cells presented CLIC1-mediated Cl^- currents. Our results suggest that CLIC1 is involved in glioma cells migration.