SOD1 and amyotrophic lateral sclerosis: Interestingly, recent findings of the Musarò Laboratory, exploiting cell-specific targeting of the SOD1 ALS mutation G93A, demonstrated that the aberrant activation of redox cascades in skeletal myocytes underlies an additional mechanism, leading to morphological alterations in the neuromuscular presynaptic terminals and neuromuscular junction (NMJ) dismantlement (Dobrowolny et al., 2018).