A recent study has shown that the SOD1 protein (whose mutations are responsible for family forms of ALS), even lacking its dismutase activity (ApoSOD1), prevents the neurotoxic effects of BMAA on cultured NSC-34 motoneurons by activating a Ca2+/Akt/Erk kinase-dependent pathway [56]. The gene discussed is SOD1; the disease is amyotrophic lateral sclerosis.