Consequently, these data show not only that structural and functional BSCB disruption is a generalized phenomenon discovered in all four ALS mouse models but also that BSCB breakdown is already detectable at stages in which there is no MN loss (P20 in SOD1G93A, P150 in FUSΔNLS/+, and P270 and P450 in Tbk1+/− mice). This evidence concerns the gene TBK1 and amyotrophic lateral sclerosis.