The first study devoted to this issue showed that inhibition of GLS, either with siRNA technology or with a specific allosteric inhibitor bis-2-(5-phenylacetamido-1,2,4-thiadiazol-2-yl)ethyl sulfide (BPTES), slowed the proliferation of human GBM D54 cells expressing mutated IDH1. Treatment with BPTES elevated levels of glycolytic intermediates, indicating alterations in the glycolytic flux [80]. The gene discussed is GLS; the disease is glioblastoma.