Although ALS-PFN1 iMGs did not exhibit deficiencies in F-actin levels or in the uptake of synaptosomes, both of which require actin polymerization, we cannot exclude the possibility that subtle alterations in cytoskeletal dynamics contribute to inefficient vesicular processing in ALS-PFN1 iMGs. This evidence concerns the gene PFN1 and amyotrophic lateral sclerosis.