SOD1 and amyotrophic lateral sclerosis: Since 1993, when SOD1 gene variants were first associated to familial ALS, more than 150 variants have been described and the mechanism of SOD1 protein dysfunction in the pathophysiology of disease was partially elucidate, and new genetic therapies are emerging from recent clinical trials and are on the verge of being used in clinical practice as innovative disease-modifying therapy for the treatment of ALS [17, 18].