Alternatively, other strategies targeting GLS isoforms have been successful in cancer cells where glutaminolysis becomes essential, as in mutant isocitrate dehydrogenase 1/2 (IDH1/2) GBM subtypes53, or in combined therapies devised to counteract the glutaminolysis-based drug resistance response, as reported in T-cell acute lymphoblastic leukemia patients treated with anti-Notch1 compounds54. Here, GLS is linked to T-cell acute lymphoblastic leukemia.