The role of zinc in ALS has been described in different ALS models and several mechanisms have been identified as possible causes of the neurotoxic alterations in zinc concentration in ALS, including higher expression of zinc-permeable calcium-permeable AMPA/kainate channels (CAK) on motor neurons [41,42], reduced levels of zinc-binding proteins metallothionein I/II and III [43], decreased zinc-binding capacity of oxidized MTs upon oxidative stress [44], down-regulated expression of ZnT3 and ZnT6 zinc transporters [17]. This evidence concerns the gene SLC30A6 and amyotrophic lateral sclerosis.