Furthermore, since pharmaceutical trials with antisense oligonucleotide capable to reduce the synthesis of mutated proteins (e.g., tofersen and jacifusen for SOD1 and FUS mutated forms, respectively) are actually ongoing, it cannot be ruled out that in the future, with a more in-depth understanding of the neurophysiopathological mechanisms addressed by NIBS techniques, ALS therapy will become multimodal, comprising both a pharmacological approach and non-invasive neurostimulation. The gene discussed is FUS; the disease is amyotrophic lateral sclerosis.