Future studies focusing on using CLIP-seq approaches for identifying differences in MATR3 wild type and mutant transcriptomic binding in the context of hnRNPM levels and/or disruption of hnRNPM-binding, particularly in neuronal cells, would be important for deciphering the mechanisms of RNA dysregulation in MATR3-ALS. The gene discussed is HNRNPM; the disease is amyotrophic lateral sclerosis.