Future studies will also need to evaluate mitochondrial transcriptional status in non-C9orf72 cases, including sporadic ALS, as well as in other forms of motor neuron disease, such as spinal muscular atrophy [14], to begin to address whether our findings are directly related to C9orf72 pathogenic mechanisms, such as dipeptide repeat proteins and/or due to, for example, TDP-43 aggregation. This evidence concerns the gene C9orf72 and spinal muscular atrophy.