This pathway is initiated by the glutaminase isozyme GLS1 (KGA) and/or its splice variant GAC (and possibly, in some cancer cases, by the glutaminase isozyme GLS2), followed by conversion of l-glutamate to α-ketoglutarate, catalyzed by α-ketoglutarate-dependent transaminases or by redox-dependent glutamate dehydrogenase (GDH). This evidence concerns the gene GLS and cancer.