The upregulation of tumoral ABAT levels in a subset of primary ACC tumors reveals a prognostically favorable inter-patient metabolic heterogeneity among the ACC cohort that also includes the upregulation of GAD1 and high expression of ALDH5A1. This “GABA shunt metabolic phenotype” is accompanied by transcript variations among genes encoding enzymes proximal to the GABA shunt that can affect the availability of glutamate for GABA synthesis. This evidence concerns the gene GAD1 and adrenal cortex carcinoma.