Lastly, given that TDP-43 pathology can also coexist with other aggregate-prone proteins, such as C9ORF72 DPRs, Tau, α-Synuclein, and poly-Q expanded Huntingtin, insight into the role of TDP-43 mislocalization in its pathogenic function will serve to better understand pathology and modes of degeneration across a spectrum of neurodegenerative diseases [184, 285–288]. This evidence concerns the gene HTT and neurodegenerative disease.