We previously showed that, in human cell lines and a mouse model, the S47 variant exhibits a modest decrease in apoptosis in response to most genotoxic stresses compared with wild-type p53, but exhibits a significant defect in cell death induced by cisplatin.8 The variant shows impaired ability to transactivate a subset of p53 target genes, including two involved in metabolism: Gls2 (glutaminase 2) and Sco2. We showed that mice expressing S47 in homozygous or heterozygous form are susceptible to spontaneous cancers of diverse histological types. Here, GLS2 is linked to cancer.