We have recently demonstrated that CLIC1 is functionally active as a chloride channel in GBM CSCs and that inhibition of CLIC1, either by gene silencing using RNA interference or by in vitro incubation with a blocking antibody, slows GBM CSC proliferation and self-renewal and reduces in vivo tumorigenicity [20]. This evidence concerns the gene CLIC1 and glioblastoma.