Intracellular hallmarks of ALS pathology comprise toxic RNA accumulation, e.g., in TDP-43, C9ORF72 and FUS mutants, impaired protein quality control leading to, e.g., aberrant folding after translation, cytoskeletal disruption, perturbed axonal organelle trafficking and mitochondrial morphology and function [11]. The gene discussed is TARDBP; the disease is amyotrophic lateral sclerosis.