Blocking RhoA/ROCK signaling can reverse the inhibitory effects of these molecules on axon outgrowth, and promotes axonal sprouting and functional recovery in animal models of CNS injury(Fujita and Yamashita 2014). As myelin and axon are the main white matter in the brain, the abnormal expression of RhoA/ROCK results in the impaired structural alterations, and further cause the functional deficits in epilepsy and other neurological disorders. The gene discussed is RHOA; the disease is epilepsy.