Moreover, in pancreatic cancer, mutant KRAS reprograms the use of glutamine-derived glutamate, such that instead of using glutamate dehydrogenase (GLUD1) to convert glutamate into α-ketoglutarate and TCA entry, glutamine-derived aspartate is converted into oxaloacetate by mutant KRAS-dependent upregulated GOT1 in the cytoplasm [74]. Here, KRAS is linked to pancreatic neoplasm.