showed that IL-8 in exosomes derived from prostate cancer cells hyperactivates peroxisome proliferators-activated receptors (PPARα) in recipient CD8+ T cells, which downregulates GLUT1 and hexokinase 2 to reduce glucose utilization while upregulating Carnitine O-palmitoyltransferase 1 and peroxisomal acyl-coenzyme A oxidase 1 to enhance fatty acid catabolism, ultimately exacerbating CD8+ T cell starvation and promoting cellular exhaustion (94). This evidence concerns the gene CD8A and prostate carcinoma.