Deactivation of Nogo-66 receptor inhibited Rho-A, thus promoting neuronal growth (McGee and Strittmatter, 2003), while NogoA neutralization inhibited Rho-A and activated Rac1 and Rho-B (Kilic et al., 2010), thus enhancing post-stroke corticospinal tract plasticity (Lindau et al., 2014). This evidence concerns the gene RHOB and stroke disorder.