In particular, L1HS expression trended toward increased expression in C9-ALS relative to control PBMCs (logFC = 0.71, pFDR = 0.075; Fig. 5C), suggesting derepression of L1HS similar to that observed in whole-blood-derived RNA from symptomatic C9orf72 HRE carriers (Fig. 4C,D). This evidence concerns the gene C9 and amyotrophic lateral sclerosis.