When initially characterizing hnRNP H-dependent splicing events, we compared C9ALS/FTD patients to neurological controls and SOD1 ALS (not believed to proceed through a mechanism of RBP dysfunction or aggregation; Ling et al., 2013), but not to sALS/FTD (Conlon et al., 2016). This evidence concerns the gene SOD1 and amyotrophic lateral sclerosis.