Two major findings of our work are: (i) downregulation of LRRC8A strongly decreases numbers of GBM cells, suggesting the importance of the LRRC8A-containing VRAC for their proliferation and viability; (ii) downregulation of LRRC8A increases sensitivity of primary GBM cells to the clinically used chemotherapeutic agents TMZ and carmustine, indicating that VRAC can be targeted for therapeutic purposes. This evidence concerns the gene LRRC8A and glioblastoma.