Research has found that a proline-arginine dipeptide repeat protein associated with C9-ALS/FTD interacts with paraspeckle components, leading to increased paraspeckle formation. This protein may cause neuronal toxicity by disrupting ribosome biogenesis. Additionally, studies using CRISPR/Cas9 to remove the ALS/FTD-causing hexanucleotide repeat expansion in C9ORF72 have shown potential to rescue disease mechanisms.