Overall, these findings suggest that RGMa in both patients and animals with ALS dephosphorylates cofilin via the RGMa/NEO1 axis, enhances actin depolymerization, resulting in the collapse of the actin barrier, and has a pivotal role in ALS pathogenesis by increasing mutant SOD1 uptake (fig. Here, NEO1 is linked to amyotrophic lateral sclerosis.