These caspase-3 levels in Ex-4 treated SOD1 (G93A) mice approached levels present in control non-ALS WT mice, suggesting that Ex-4 inhibited caspase-3-mediated apoptosis in SOD1 (G93A) mice, and providing a potential mechanism to account for the described motor neuron protection. The gene discussed is SOD1; the disease is amyotrophic lateral sclerosis.