Transgenic SOD1-ALS mice showed increased levels of STMN1 and STMN2 in the spinal cord, and overexpression of both STMN1 and STMN2 in NSC-34 MNs has been proved to induce microtubule defects leading to Golgi fragmentation [16]. The gene discussed is STMN2; the disease is amyotrophic lateral sclerosis.