Previously, we and others have shown that loss of TMEM106B results in age-dependent-ALS/FTLD related pathological changes, including an increase in the levels of ubiquitinated proteins, autophagy adaptor protein p62, and phosphorylated TDP-43 in both the brain and the spinal cord [13, 25]. This evidence concerns the gene TMEM106B and amyotrophic lateral sclerosis.