Loss of function due to mislocalization results in a loss of VPS4B repression leading to an increased interaction with the ALS-linked protein Charged Multivesicular Body Protein 2B (CHMP2B) thereby disrupting dendritic recycling-endosome trafficking and reducing ALS-linked ERB-B2 Receptor Tyrosine Kinase 4 (ERBB4) surface expression [191–193]. This evidence concerns the gene CHMP2B and amyotrophic lateral sclerosis.