While axonal transport defects may contribute to disease in KIF5A cases, and potentially in others influencing cytoskeleton or motor proteins such as dynactin subunit 1 (DCTN1), neurofilament proteins (NF-L, NF-H), spastin (SPAST) and tubulin alpha 4a (TUBA4A) [94], the wider role of axonal transport deficits in ALS remains unknown. This evidence concerns the gene KIF5A and amyotrophic lateral sclerosis.