SOD1 and amyotrophic lateral sclerosis: In the same paper, Jag1 deletion was found to aggravate disease progression in an ALS mouse model that over-expresses mutant SOD1. Although these studies suggest that the Notch pathway is likely aberrantly regulated in ALS patient brains and manipulations of the pathway can modulate disease-related phenotypes in multiple model systems, additional studies are required to determine whether Notch signaling aggravates or suppresses disease progression before translating these findings to clinical care.