The events discussed above can lead to impairment of fast and slow axonal transport in vivo that has been well established in adult SOD1 mutant mice (Collard et al. 1995; Zhang et al. 1997; Warita et al. 1999; Williamson and Cleveland 1999; Sasaki et al. 2004; Ligon et al. 2005) and in human ALS patients (Bradley et al. 1983) deficits have even been reported in cultured embryonic MNs from SOD1 mice (Kieran et al. 2005; De Vos et al. 2007). The gene discussed is SOD1; the disease is amyotrophic lateral sclerosis.