Stathmin, a phosphoprotein that promotes microtubules depolymerization, and MAP1B, a microtubule-associated protein regulating α-tubulin detyrosination, are up-regulated in murine cellular SMA models, and their depletion restores proper mitochondrial transport and localization, as well as ameliorate SMA phenotypes [66,87]. The gene discussed is SMN1; the disease is proximal spinal muscular atrophy.