Researchers have observed that ALS patients with a FUS mutation experience abnormalities such as cytoplasmic FUS localization, axonal transport defects, and an altered association between cells' mitochondria and endoplasmic reticulum (ER). The silencing of HDAC6 through gene therapy appears to correct the latter two defects. Therefore, researchers are exploring gene therapies that would inhibit the production of HDAC6 as a means of treating ALS symptoms or preventing it from progressing.