Evidence for the opposing roles of Bcl-2 and Bax in ALS has been obtained through the overexpression of Bcl-2, which enhances motor neuron survival and delays onset of the disease (Kostic et al., 1997; Azzouz et al., 2000; Vukosavic et al., 2000). The gene discussed is BCL2; the disease is amyotrophic lateral sclerosis.