ACOX1 upregulation may stabilize β-catenin via palmitoylation, activating proliferation-related signaling [37]; high ACC1 expression inhibits fatty acid oxidation by producing malonyl-CoA, helping maintain tumor energy homeostasis [38]; and CD36 activation enhances uptake of exogenous long-chain fatty acids and promotes EMT and angiogenesis through PPARγ and NF-κB pathways [39]. The gene discussed is ACACA; the disease is neoplasm.