In reverse, as an interplay communication, some pro-inflammatory cytokines such as IL-6 and TNF-α have high levels in the spinal cord, which when under GMD conditions, can accelerate the release of growth-associated protein 43 (GAP-43), neurotrophin-3 (NT-3) and BDNF from the brain neurocytes, and then modulate the axonal plasticity to spontaneously attenuate the IS-derived brain injuries (70). This evidence concerns the gene NTF3 and brain injury.