Furthermore, deriving a gene signature of sensitivity towards GLS1 inhibition verified in patient-derived xenograft (PDX) models allowed the authors to predict a higher sensitivity towards inhibiting GLS1 (given a high expression of GAC, a tumour-specific splicing isoform of GLS1) and γ-glutamylcysteine synthetase (an enzyme responsible for glutathione synthesis) in mesenchymal tumours among different cancers (reviewed in ref. 139). Here, GLS is linked to mesenchymal cell neoplasm.