CRAT (carnitine O-acetyltransferase) is a key mitochondrial enzyme that catalyzes the reversible transfer of acetyl groups between acetyl-CoA and carnitine, maintaining optimal mitochondrial carbon flux and preventing acetyl-CoA accumulation 1. This bidirectional enzyme is responsible for synthesizing short- and branched-chain acylcarnitines 2 and plays a crucial role in transporting fatty acids for beta-oxidation 34. CRAT regulates the acyl-CoA/CoA ratio and contributes to metabolic flexibility by buffering the balance between fatty acid and glucose oxidation 1. Under calorie restriction, CRAT expression is upregulated, supporting increased acetylcarnitine and short-chain acylcarnitine production, facilitating acetyl group distribution across cellular compartments 5. CRAT localizes primarily to mitochondria, with alternative transcripts potentially targeting other compartments 6. Clinically, CRAT dysfunction is associated with mitochondrial encephalopathy and Leigh syndrome; missense variants impairing catalytic function toward acetyl-CoA and branched-chain substrates cause carnitine acetyltransferase deficiency 7. Additionally, genetic polymorphisms in CRAT influence carnitine metabolism in red blood cells, affecting lipid damage repair and age-dependent hemolysis 8.