From the original ALS mouse model representing the familiar form of ALS with the mutation of the superoxide dismutase 1 (G93A‐SOD1) gene,5 a growing number of rodent models that express different mutations, such as the fused in sarcoma (FUS),6 the C9orf72 hexanucleotide repeat expansion mice,7, 8 and the transactive response DNA binding protein 43 kDa TDP‐439, 10 (among others) have been increasingly developed to address the effects of molecular changes on neuronal degeneration and death. This evidence concerns the gene C9orf72 and amyotrophic lateral sclerosis.