Bacterial pore-forming toxins induce a rapid and massive increase in cytosolic Ca²⁺ concentration due to the formation of pores in the plasma membrane and/or activation of Ca²⁺-channels. As Ca²⁺ is an essential messenger in cellular signaling, a sustained increase in Ca²⁺ concentration has dramatic consequences on cellular behavior, eventually leading to cell death. However, host cells have adapted mechanisms to protect against Ca²⁺ intoxication, such as Ca²⁺ efflux and membrane repair. The final outcome depends upon the nature and concentration of the toxin and on the cell type. This review highlights the repercussions of Ca²⁺ overload on the induction of cell death, repair mechanisms, cellular adhesive properties, and the inflammatory response.