While treatments which elevate 2-pyrrolidinone levels through GABA-transaminase inhibition can interfere with the use of 2-pyrrolidinone as a biomarker for screening GABA-transaminase deficiency, the treatment of patients with these drugs can be discerned from the patient medical history, and many of these medications can also be detected in clinical metabolomic analysis of plasma. This evidence concerns the gene ABAT and GABA aminotransaminase deficiency.