In addition to inhibiting the aggregation and transit of the TDP-43 protein to SGs, highly dynamic intracellular accumulations of protein and RNA that are thought to play a role in ALS-FTD29,47,48, we demonstrate that this class of CRISPR-based proteins can be harnessed to slow disease progression in vivo. This evidence concerns the gene TARDBP and amyotrophic lateral sclerosis.