Life has evolved around Zn and so apparently has the regulation of cell division and cell death. An increase in cytosolic Zn during mid-G1 is essential for the induction of cyclins and other gene products required for the cell to prepare for replication of its DNA. A second requirement for Zn precedes mitotic division of the cell. A role for the action of specific Zn transporters in mitosis is rapidly emerging. The relationship of Zn to cell death is intriguing as this metal ion can both suppress and promote apoptosis, depending upon factors which are still poorly understood. Zn protects many types of cell from oxidant-induced apoptotic cell death by, amongst other things, inhibiting events leading to activation of the caspase executioner proteins. Recent studies showing a role for Zn in macrophage phagocytosis suggests impaired efferocytosis as an alternative mechanism by which apoptotic cells can accumulate in the tissues in Zn deficiency. Under some circumstances, Zn acts as a potent inducer of apoptosis, such as in neurons dying during seizures and brain injury where it contributes to pathogenesis. Other emerging mechanisms of cell death, including autophagy and pyroptosis, are also influenced by Zn and Zn deficiency. In addition to the above roles of Zn as either a suppressor or promoter of cell death, a general feature of apoptosis and autophagic cell death is a substantial increase in fluorophore-detectable, labile Zn within the dying cell's cytoplasm or vacuoles, respectively; the significance of this Zn release is not known. The dual roles of Zn in regulating cell proliferation and cell death point to a pivotal role for this metal ion in tissue homeostasis with important implications for diseases in which the delicate balance between cell birth and cell death goes amiss.