For instance, CPT1A-mediated fatty acid oxidation promotes cell proliferation via nucleoside metabolism in nasopharyngeal carcinoma.28 Disruption of CPT1A through genetic or pharmacologic ways can cut off the supply of NADPH, thus preventing anchor-independent growth of ESCC cells and lung metastasis.29 Recently, CPT1A was identified as a succinyltransferase. The gene discussed is CPT1A; the disease is esophageal squamous cell carcinoma.