In summary, we have demonstrated that sustained renal ROS overproduction after burn induced continuous tubular cell apoptosis and thus a late ARF, which may result from ROS-mediated activation of p38 MAPK but a late inhibition of Akt phosphorylation in severely burned rats, and that anti-oxidative treatment may represent a promising potent therapy in clinical applications of late ARF after burn. This evidence concerns the gene AKT1 and acute kidney injury.