Lipid overload increased the levels of FAs in cells and was associated with elevated β-oxidation, lipid peroxidation, mitochondrial damage, ER stress, impaired insulin signaling, increasing inflammatory mediators, and cell death, which may account for parts of reasons why SLC27A6-mediated lipid overload inhibited tumor growth in NPC. This evidence concerns the gene SLC27A6 and nasopharyngeal carcinoma.