GLS1 has two splice variants: kidney‐type glutaminase (KGA), and glutaminase C (GAC).12 This metabolic transformation is the result of complex interactions between a hypoxic tumor microenvironment and oncogenic mutations, such as epidermal growth factor receptor (EGFR), TP53 and Kirsten rat sarcoma viral oncogene (KRAS).9, 13, 14, 15, 16 Higher glucose utilization correlates with aggressive tumor behavior and treatment resistance including radiotherapy.6 Therefore, tumor metabolism might be exploited in future treatment strategies. The gene discussed is TP53; the disease is neoplasm.