Recently, an elaborate biochemical study with purified ZnT8 variant proteins showed that the common high-risk p. R325 variant is hyperactive and exhibits accelerated zinc transport kinetics compared with the p. W325 variant associated with a lower risk96, which contradicts previous conclusions from rodent tumor cell lines, but is consistent with human genetic results that the rare loss of function ZnT8 mutations decreases the risk of diabetes. This evidence concerns the gene SLC30A8 and diabetes mellitus.