Nonetheless, no consensus has yet emerged as to how SOD1 mutations lead to selective death of motor neurons, except that multiple toxicity pathways including oxidative stress, endoplasmic reticulum (ER) stress, excitotoxicity, mitochondrial dysfunction, neural inflammation, protein misfolding and accumulation, and dysfunctional intracellular trafficking, are implicated in the pathogenesis of ALS/MNDs [1], [24]. The gene discussed is SOD1; the disease is amyotrophic lateral sclerosis.