EAAT2/G93A mSOD1 double Tg mice showed moderate amelioration of the ALS-like phenotype with a statistically significant (14 days) delay in grip strength decline and loss of motor neurons as well as a reduction in other events including caspase-3 activation and SOD1 aggregation but not in the onset of paralysis, body weight decline or an extended life span when compared with monotransgenic G93A mSOD1 littermates (Guo et al., 2003). The gene discussed is SOD1; the disease is amyotrophic lateral sclerosis.