Therefore, our computational study provides a molecular insight to the recent GWAS findings6 in that loss-of-function of ZnT8 and subsequent Zn2+ deficiency in β-cell granules shift the insulin oligomer equilibrium toward insulin monomers and dimers, which bind IAPP monomers efficiently and prevent IAPP from self-association and aggregation, thus reducing T2D risk. The gene discussed is SLC30A8; the disease is type 2 diabetes mellitus.