In the last decade, proteomic studies performed on different in vitro models, have highlighted microglial dysfunction and mitochondrial impairment as key contributors in disease pathogenesis,77-80 demonstrated cryptic exons translation into new peptides in TDP-43-depleted cellular models,81 and shed light on defects in cellular transport mechanisms82,83 and protein interaction networks through advanced interactomics,36,84,85 contributing to increase our understanding on ALS. Here, TARDBP is linked to amyotrophic lateral sclerosis.