In particular, in motor neurons that survived the disease process in human SOD1-related ALS, anti-apoptotic phosphatidylinositol 3-kinase and protein kinase B (AKT3) were up-regulated with a concomitant reduction in the level of phosphatase and tensin homologue (PTEN) which inhibits the pro-survival AKT pathway, suggesting a mechanism for how these intact motor neurons survived the neurodegenerative process. The gene discussed is AKT1; the disease is amyotrophic lateral sclerosis.