FUS and amyotrophic lateral sclerosis: A third, more direct strategy employs targeted degradation, using tools like antisense oligonucleotides (ASOs) to reduce the synthesis of the problematic protein (e.g., ION363 targeting FUS in ALS) or proteolysis-targeting chimeras (PROTACs) to promote its destruction (e.g., targeting BRD4, a component of transcriptional condensates) [59,60].