All of these data, combined with the promising outcomes reported in clinical studies in ALS patients treated with Lithium [20], the first GSK-3β inhibitor identified, suggest that the gain of function of GSK-3β due to the aberrant expression and/or activation could be one of the pathogenic mechanisms of ALS, considering GSK-3β a potential therapeutic target for this devastating neurodegenerative disease. This evidence concerns the gene GSK3B and neurodegenerative disease.