HDAC6 and amyotrophic lateral sclerosis: Interestingly, approaches for rescuing axonal transport defects through microtubule stabilization were frequently considered putative therapeutic targets in ALS therapy in general but also specifically in FUS-ALS, e.g., by manipulating post-translational modifications in microtubules via silencing HDAC-6 by antisense oligonucleotides in MNs derived from mutant FUS patients [14,55].