In addition, upregulation of FA transporter-binding protein 4 (FABP4) and G protein-coupled receptor 84 (GPR84) expression on the surface of effector and memory CD8+ T cells in RA patients concomitantly increases FA uptake, and further blocking FA metabolism in vitro would seriously impair the effector function of CD8+ T cells and further in vitro blockade of FA metabolism would severely impair the effector function of CD8+ T cells [74]. This evidence concerns the gene CD8A and rheumatoid arthritis.