The increase in intracellular free Zn2+ is thought to originate from intracellular stores (mainly the endoplasmic reticulum) but it remains to be seen whether sporadic increases in extracellular free Zn2+ might also contribute to this regulatory mechanism, and whether and how the Zn-FFA crosstalk via albumin contributes to systemic zinc dyshomeostasis in metabolic syndrome and type 2 diabetes. This evidence concerns the gene ALB and type 2 diabetes mellitus.