This also indicates that TBI could be sufficient to exacerbate the phenotypes associated with ALS-causing genes, in this case C9orf72. In the same study, Anderson and colleagues demonstrated the deposition of ubiquitin, p62/SQSTM1, TDP-43, and stress granule formation within the Drosophila brain following repetitive trauma and, interestingly, Drosophila with repeated brain trauma exhibited highly similar pathology to that observed in ALS patients and ALS mouse models [175]. This evidence concerns the gene TARDBP and amyotrophic lateral sclerosis.