PROK2 and experimental autoimmune encephalomyelitis: We have recently demonstrated that peripheral nerve injury causes a dramatic increase of PROK2 in DRG neurons and in activated astrocytes in the spinal cord, associated with development of neuropathic pain22 and identified PROK2 as a critical mediator of experimental autoimmune encephalomyelitis (EAE), animal model of Multiple Sclerosis25.