Such training prevents atrophy of spinal motoneurons in SCI [21], inhibits neuronal apoptosis by activating cyclic adenosine monophosphate/protein kinase A (cAMP/PKA), protein kinase B (Akt), and glycogen synthase kinase 3beta (GSK3β) pathways in rat brains post-ischemia [22], and promotes the sprouting of lateral axon branches in SCI [23], as well as axonal regeneration in peripheral nerve damage [24]. The gene discussed is AKT1; the disease is ischemia.