Moreover, as we have previously discussed, the co-localisation of p62 to DPRs, specifically poly-GA which sequesters Unc119 [22], highlights the complex and potentially synergistic effects of both reduction in C9orf72 protein levels and DPR expression in dendritic and axonopathy and the pathogenesis of C9-ALS/FTD [11, 22, 30, 31, 81, 85]. The gene discussed is C9; the disease is amyotrophic lateral sclerosis.