Elevated levels of IL-6 and TNF-α in the spinal cord after stroke upregulate the concentrations of GAP-43 (growth-associated protein 43), NT-3 (neurotrophin-3), and BDNF, all of which are known to be involved in spinal axonal plasticity and lead to better spontaneous post-stroke recovery (39). The gene discussed is GAP43; the disease is stroke disorder.