These results provide substantial evidence for a non-cell autonomous effect mediated by glia (Ilieva et al., 2009) that is similar to that reported when glial cells from G93A-SOD1 transgenic mice are co-cultured with motor neurons (Nagai et al., 2007) and indicates that glial-motor neuron interactions play an important role in ALS pathogenesis. The gene discussed is SOD1; the disease is amyotrophic lateral sclerosis.