Interestingly, the targets we found to have enhanced interaction with both MATR3 and hnRNPM in cells expressing disease-causing mutations in MATR3, including DYRK1A and SMYD3, are also prime RNA targets of other ALS-associated RBPs, FUS and TDP-43, and additionally, have been associated with RNA dysregulation in ALS [56–61]. This evidence concerns the gene HNRNPM and amyotrophic lateral sclerosis.