Moreover, unlike neurons treated with Sol8-vector, Western blot analysis demonstrated that the signal intensity of phosphorylated Cofilin at S3 (p-Cofilin-S3), which is a hallmark of growth cone collapse in neuronal cells, as well as a marker of reduced axonal actin dynamics in ALS patients with depleted and mutated C9ORF72 (Heredia et al., 2006; Sivadasan et al., 2016), was upregulated in neurons treated with Sol8-NogoA CM (Figure 1—figure supplement 1). The gene discussed is RTN4; the disease is amyotrophic lateral sclerosis.