Indeed, a study using the transient MCAO stroke model showed that AMPH-enhanced poststroke motor performance of rats was accompanied with a transient increase in FGF-2 expression in layer V sensorimotor neurons in the unlesioned cortex at 2 weeks poststroke, along with enhanced axonal sprouting across the midline from the unlesioned cortex (Wolf et al., 2014). This evidence concerns the gene FGF2 and stroke disorder.