Research from Italy indicates that N-type Ca2+ channels contribute to the pathogenesis of amyotrophic lateral sclerosis (ALS). These channels were found to be overexpressed in cortical neurons and motor cortical tissue from mice with the ALS-related mutation Gly93Ala in the SOD1 gene. Compared with control cells, Gly93Ala cortical neurons showed increased calcium entry during depolarization, as well as reduced survival—an effect that was reversed by addition of an N-type Ca2+ channel blocker.