CD36 overexpression enhances FAs uptake and intracellular lipid deposition in tumor cells, accordingly fueling tumor progression [128]; FABP5 overexpression drives epithelial-mesenchymal transition (EMT) and promotes lymphatic metastasis through FAs metabolic reprogramming, thereby facilitating tumor immune evasion [129]; and FATP2 functions as a LCFA transporter, facilitating intracellular lipid influx, particularly of arachidonic acid, the precursor of prostaglandin E2, which plays a key role in tumor-associated inflammation [130]. The gene discussed is FABP5; the disease is neoplasm.