CPT2 (carnitine palmitoyltransferase 2) is a mitochondrial enzyme essential for fatty acid β-oxidation that reconverts acylcarnitines back into acyl-CoA esters, enabling long-chain fatty acids to undergo β-oxidation within mitochondria 1. The enzyme is active with medium (C8-C12) and long-chain (C14-C18) acyl-CoA esters and plays a crucial role in maintaining cellular energy homeostasis through fatty acid metabolism. CPT2 activity is regulated by post-translational modifications, particularly succinylation at Lys424, which when increased leads to enzymatic inactivation and accumulation of fatty acyl-carnitines 2. Dysregulation of CPT2 has significant pathological implications across multiple diseases. Downregulation occurs in obesity-driven hepatocellular carcinoma, where it enables cancer cells to escape lipotoxicity and promotes carcinogenesis through acylcarnitine accumulation 1. In ischemic stroke, CPT2 deficiency leads to harmful acylcarnitine buildup that damages astrocytic mitochondria and compromises neuronal support 3. The enzyme is also implicated in glioblastoma radioresistance, where fatty acid oxidation pathways including CPT2 fuel tumor survival 4. Clinically, CPT2 deficiency causes inherited metabolic disorders ranging from mild myopathy to severe neonatal forms, while therapeutic targeting shows promise for diabetic cardiomyopathy and cancer treatment 5.