Other articles focus on the C9orf72 gene mutation and its related mechanism, revealing the important role of GGGGCC repeat amplification in C9orf72 gene in the pathogenesis of FTLD-ALS and the neurotoxicity mechanism of the resulting dipeptide-repeat proteins (DPRs).[32–34] These studies further enriched the pathological spectrum of FTLD-ALS and provided new directions for the diagnosis and treatment of hereditary FTLD-ALS. Here, C9orf72 is linked to amyotrophic lateral sclerosis.