In a separate case, circular RNAs have been proposed as therapeutic agents [196]: in this study depleting the lariat-debranching enzyme Dbr1 was shown to block the cytotoxic effects exerted by an ALS-causing mutant version of the TDP43 RNA-binding protein, and the authors suggested that the reason for this welcome effect was that the increased pool of unprocessed circular intronic lariats (after Dbr1 depletion) sequestered the mutant TDP43 [196]. This evidence concerns the gene DBR1 and amyotrophic lateral sclerosis.