Interestingly, many amyotrophical lateral sclerosis/frontotemporal dementia (ALS/FTD)-linked mutations on several RBPs (e.g., TDP43, FUS, TIA1) drive the formation of aberrant SGs both in vitro and in vivo suggesting that mRNA mislocalization and/or loss of RBP function may be a common feature of pathogenic mechanisms in neurodegeneration (discussed in [6]). This evidence concerns the gene TIA1 and amyotrophic lateral sclerosis.