Interestingly, the chronic elevation of oxidative stress in FRDA patients and animal models may be a contributing factor in the activation of cytokines responsible for COX2 overexpression (8–12), suggesting the mechanism fxn-deficiency->ROS->cytokines->CREB/AP1->COX2->iba1/microglial activation->neuroinflammation->neurodegeneration (Fig. 8). The gene discussed is JUN; the disease is Friedreich ataxia.