The recent observations of augmented glutamate exocytosis in Mcoln1−/− KO neurons [15] and enhanced loading of glutamate into zinc-rich vesicles by ZnT3 and Vglut1 proteins [11] lend further credence to the possibility that decreased Slc30a3/ZnT3 expression in certain brain disorders may be a negative feedback regulation to prevent or minimize both glutamate and zinc-induced cytotoxicity. This evidence concerns the gene SLC30A3 and brain disorder.