GATB (glutamyl-tRNA amidotransferase subunit B) is a mitochondrial enzyme subunit essential for aminoacyl-tRNA biosynthesis. As part of the glutamyl-tRNA amidotransferase complex, GATB catalyzes the transamidation of misacylated Glu-tRNA(Gln) to generate correctly charged Gln-tRNA(Gln) in mitochondria, utilizing glutamine and ATP as substrates 1. This indirect pathway for glutaminyl-tRNA synthesis is critical for proper mitochondrial translation. GATB function has been demonstrated across diverse organisms; in Plasmodium parasites, GATB forms a heterodimeric complex with GatA and is essential for erythrocytic stage viability 1. In humans, GATB dysfunction is associated with combined oxidative phosphorylation deficiency 41 (COXPD41), reflecting the critical role of correct tRNA aminoacylation in mitochondrial respiratory chain assembly. Beyond its canonical function, GATB has been identified as a genetic risk locus in genome-wide association studies. In African ancestry populations, a variant in the GATB/FHIP1A region showed significant association with LDL cholesterol levels 2, and African ancestry-specific variants near PET112/GATB were associated with suicidal thoughts and behaviors 3. These findings suggest GATB involvement extends beyond mitochondrial translation to influence complex physiological and psychiatric phenotypes.