To confirm that the increased XO activity in Depdc5-deficient CD8+ T cells was responsible for elevated ROS production and lipid peroxidation, we treated WT and Depdc5-deficient CD8+ T cells either with vehicle or well-known XOR inhibitor allopurinol (which is in frequent clinical use for the treatment of gout, a metabolic disease linked with enhanced purine metabolism)57. The gene discussed is CD8A; the disease is metabolic disease.