Bevacizumab has been shown to diminish injury in the experimental autoimmune encephalomyelitis model of MS by suppressing angiogenesis, suggesting that VEGF may play some part in the development of MS [80], Argaw et al. suggested that astrocytes might represent an important source of VEGF-A, which leads to the activation of eNOS and plays a significant role in the loss of BBB that occurs in MS [42]. This evidence concerns the gene NOS3 and myeloid sarcoma.