CD8+ T cells in the blood of patients with RA meet their metabolic requirements through aerobic glycolysis, and inhibition of LDHA by using FX11 resulted in decreased adipogenesis, CD8+ T cell migration and proliferation, and CD8+ T cell effector function, increased ROS production, and loss of their ability to induce healthy B cells to develop a pro-inflammatory phenotype [73]. The gene discussed is CD8A; the disease is rheumatoid arthritis.