CPT1Α not only promotes lipid consumption through the fatty acid metabolic pathway, thereby reducing lipotoxicity, but also anchoring Bcl2 to the mitochondrial membrane, thereby preventing cytochrome C release and inhibiting the mitochondrial apoptotic process (Xie, et al. 2024) In CPT1a-null lung cancer cells, reduced NADPH and reduced glutathione were observed, while free fatty acid levels were increased. This evidence concerns the gene CYCS and lung cancer.