Thus, despite different underlying genetic causes and presentation of TDP43 pathology (as in the case of SOD1 and FUS), it appears that common synaptic alterations do not represent a random event but rather a key pathological feature shared across the ALS spectrum at the proteomic, but also transcriptomic and even epigenetic level [13]. This evidence concerns the gene TARDBP and amyotrophic lateral sclerosis.