Neuronal capability to cope with OS is limited, since low expression of antioxidant defense regulators, such as nuclear factor-erythroid factor 2-related factor 2(Nrf2) and peroxisome proliferator-activated receptor-gamma co-activator (PGC)-1a, seems to take place, especially during the progressive MS, whereas gene deletions in mitochondria may associate with energy deficiency, calcium ions imbalance, axonal degeneration and apoptosis of neurons and oligodendrocytes, that due to the high iron storage may be enhanced together with the radical formation via the Fenton reaction [29]. Here, NFE2L2 is linked to myeloid sarcoma.