Future research using animal models is needed to further our understanding of the PARP-dependent mechanism of FUS condensate formation in the nucleus, as well as FUS functions downstream of nuclear PARPs, such as the involvement of FUS in the organization of DNA repair compartments, the assembly of stress granules or the accumulation of cytoplasmic FUS inclusions, which are a hallmark of frontotemporal lobar degeneration and amyotrophic lateral sclerosis. This evidence concerns the gene PARP1 and frontotemporal dementia.