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Ca²⁺ is an important second messenger participating in many cellular activities; when physicochemical insults deregulate its delicate homeostasis, it acts as an intrinsic stressor, producing/increasing cell damage. Damage elicits both repair and death responses; intriguingly, in those responses Ca²⁺ also participates as second messenger. This delineates a dual role for Ca²⁺ in cell stress, making difficult to separate the different and multiple mechanisms required for Ca²⁺‐mediated control of cell survival and apoptosis. Here we attempt to disentangle the two scenarios, examining on the one side, the events implicated in deregulated Ca²⁺ toxicity and the mechanisms through which this elicits reparative or death pathways; on the other, reviewing the role of Ca²⁺ as a messenger in the transduction of these same signaling events.