We also showed that some REST-null clones were able to rewire fatty acid metabolism to derepress their growth and that this compensation effect could be negated using a chemical inhibitor of long-chain acyl-CoA synthetases, Triacsin C. GR-28 exhibited profound synergy when combined with Triacsin C in GBM cells, but not in hepatocarcinoma cells (HepG2), allowing effective eradication of glioblastoma cells with limited hepatotoxicity in vitro. This evidence concerns the gene REST and glioblastoma.