Additionally, post-mortem analyses demonstrated MATR3 pathology—consisting of cytoplasmic MATR3 accumulation as well as strong nuclear immunostaining—in patients with sporadic ALS and familial disease due to C9orf72 hexanucleotide expansions and FUS mutations (Dreser et al., 2017; Tada et al., 2018). The gene discussed is FUS; the disease is amyotrophic lateral sclerosis.