Previously, we found that the N-terminal LCR of FUS/TLS (Translocated in Liposarcoma) mediates co-aggregation with mutant huntingtin (Htt)31 and later identified FUS/TLS as a tightly bound component of the Htt aggregates in vivo using Htt aggregates isolated from Huntington disease model mice32. This evidence concerns the gene HTT and liposarcoma.