GLS2 and breast cancer: A comparison of the metabolic phenotype and the gene expression between mesenchymal and epithelial breast tumor cells illustrates that the loss of GLS2 expression upon the induction of EMT leads to enhanced glutamine-independent phenotype and reduced mitochondrial activity, while the restoration of GLS2 expression in GLS2-negative breast cancer cells increases mitochondrial glutamine consumption and suspends BCSC-like properties (Ramirez-Peña et al., 2019).