Focusing on the familial ALS forms, one of the most investigated genetic mechanism is the mutation of glycine 93 in alanine (G93A) in the Cu/Zn Superoxide Dismutase-1 (SOD1) gene (Chen et al., 2013), whereas in sporadic forms the Transactive Response DNA binding protein (TDP-43) has been identified as the major pathological molecular determinant (Halliday et al., 2016). The gene discussed is SOD1; the disease is amyotrophic lateral sclerosis.