For the familial forms, several genetic mutations have been identified as being associated with the disease, including mutations in Cu superoxide dismutase (SOD1), TAR DNA binding protein-43 (TDP-43), the C9orf72 gene (the most common mutation underlying familial forms of ALS), and the recently discovered TBK1 gene encoding a protein involved in two essential cellular pathways of emerging interest in ALS research: autophagy and inflammation [4]. Here, TARDBP is linked to amyotrophic lateral sclerosis.