Given the importance of understanding the molecular basis for the connection between ZnT-8 and altered diabetes susceptibility we recently investigated the effect of a global deletion of Slc30a8, in the context of mice with a mixed C57BL/6J×129SvEv genetic background, to address the hypothesis that the absence of ZnT-8 results in impaired islet function and thereby contributes to type 2 diabetes. The gene discussed is SLC30A8; the disease is type 2 diabetes mellitus.