Nevertheless, earlier studies, chiefly performed on homozygous ZnT8 KO mice [reviewed in (14)] demonstrate poorer glucose homeostasis versus wild-type littermates, especially on diabetes-prone backgrounds (e.g., human islet amyloid polypeptide, IAPP-transgenic mice) (16), or after high fat feeding (36). The gene discussed is SLC30A8; the disease is diabetes mellitus.