Using a similar approach, it has been demonstrated that inactivation of NF-κB activity in astrocytes can either protect neurons from different insults (improving functional recovery following spinal cord injury [33], [34] and experimental autoimmune encephalomyelitis [35], and promoting survival of retinal neurons following ischemic injury [36]), or have no effect on preventing neuronal death in cerebral ischemia [37]. This evidence concerns the gene NFKB1 and experimental autoimmune encephalomyelitis.