Targets were selected on the basis of direct links to ALS/FTD or other neurological diseases (e.g. ATXN2, KIF1C, PEX19, ARRB2), or because of documented involvement in pathways implicated in ALS/FTD such as excitotoxictiy (GABBR1, CABIN1), protein degradation (PSMD4, BAT3), cytoskeletal remodeling and neuritogenesis (PPP1R12C) and RNA metabolism (PAN2, RNH1, DAZAP1). This evidence concerns the gene ATXN2 and amyotrophic lateral sclerosis.