CPT1A (carnitine palmitoyltransferase 1A) is the rate-limiting enzyme for mitochondrial fatty acid oxidation, catalyzing the conversion of long-chain fatty acid-CoA conjugates to acyl-carnitines for mitochondrial uptake and subsequent β-oxidation 1. Beyond its classical metabolic role, CPT1A exhibits non-canonical functions including lysine succinyltransferase activity that can regulate substrate proteins 2. In cancer contexts, CPT1A promotes tumor cell survival through metabolic reprogramming, facilitating lipid droplet-mitochondria tethering to enhance β-oxidation during energy stress 3. CPT1A also supports radioresistance in glioblastoma by driving fatty acid oxidation that upregulates CD47-mediated immune evasion 4. Conversely, CPT1A plays beneficial roles in immune function by recruiting ZDHHC4 to palmitoylate MAVS, stabilizing the type I interferon response and enhancing antitumor immunity 5. In natural killer cells, fasting-induced CPT1A upregulation improves anti-tumor responses through enhanced fatty acid metabolism 6. However, CPT1A activation in hepatic stellate cells promotes liver fibrosis, making it a potential therapeutic target 7. The enzyme's regulation involves multiple layers including genetic, epigenetic, and nutritional modulators, with dysregulation associated with metabolic disorders and cancer 1.