[5][6][7][8][9][10] FUS/TLS was initially identified as a fusion protein (FUS-CHOP) produced as a result of chromosomal translocations in human cancers, especially liposarcomas.

[24] Beyond nucleic acid binding, FUS/TLS was also found to associate with both general and more specialized protein factors to influence the initiation of transcription.

[29][30][31] Recently, FUS/TLS was also shown to repress the transcription of RNAP III genes and to co-immunoprecipitate with TBP and the TFIIIB complex.

[33] The function of FUS in the DNA damage response in neurons involves a direct interaction with histone deacetylase 1 (HDAC1).

Mutations in the FUS nuclear localization sequence impairs the poly (ADP-ribose) polymerase (PARP)-dependent DNA damage response.

[35] In 2009 two separate research groups analysed 26 unrelated families who presented with a type6 ALS phenotype, and found 14 mutations in the FUS gene.

FTD differs from the more common Alzheimer's dementia in that memory is relatively well preserved; instead, the disease presents with a more temporal-lobe phenotype.