<prompt> Answer this question truthfullyCould you provide me with the existing sentence so I can better understand how to rephrase it in proper English?  <response>: <reason> FTLD is strongly familial, with up to 40 of patients having a history of a similar disorder within their family, indicating that genetic factors play a significant role in its etiology. An autosomal dominant pattern of inheritance is documented in about 10. Three significant causal genes have been identified. Mutations in MAPT on chromosome 17 71,160, not unexpectedly, drive FTLD-tau pathology. FTLD-TDP pathology, by contrast, is not, or perhaps only rarely, associated with mutations in the TDP-43 gene, TARDBP. Instead, it is represented by mutations in the progranulin gene GRN on chromosome 17 9,34 or expansions in C9orf72 on chromosome 9 40,134. Mutations in other genes have also, less commonly, been associated with FTLD. Of these, most notable are CHMP2B mutations on chromosome 3 20,56,148 occurring almost exclusively within a single pedigree within the Jutland region of Denmark 20,56,74. NCI is present in such cases, and although these are ubiquitinated, the target protein remains to be identified. The classification, FTLD-UPS, has been applied in recognition of the involvement of the ubiquitin-proteasome system in the disease. The vast majority of cases with FTLD-FUS pathology appear to be sporadic. Other rare genetic forms of FTLD involve mutations in valosin containing protein VCP 174, SQSTMI also known as p62, optineurin OPTN 104, ubiquitin 2 UBQLN2 and TANK binding-kinase 1 TBK1. Although collectively, such cases are numerically few, they do provide essential clues to pathogenesis since all involve TDP-43 proteinopathy, and all have functioned within the cells protein degradation systems. 