Similarly, pancreatic ductal adenocarcinoma (PDAC) harbors stem-like cells that heavily depend on glutamine metabolism to fuel the tricarboxylic acid (TCA) cycle and maintain redox balance under nutrient-limited conditions.272,273 Interfering with glutamine utilization, such as via pharmacological inhibition of glutaminase (GLS) or disruption of key transporters, can selectively deplete CSCs in PDAC xenograft models. This evidence concerns the gene GLS and pancreatic ductal adenocarcinoma.