As with other complex cellular functions, intracellular membrane transport involves the coordinated engagement of a series of organelles and machineries; in the last couple of decades more importance has been given to the role of calcium (Ca(2+)) in the regulation of membrane trafficking, which is directly involved in coordinating the endoplasmic reticulum-to-Golgi-to-plasma membrane delivery of cargo. Consequently, the Golgi apparatus (GA) is now considered not just the place proteins mature in as they move to their final destination(s), but it is increasingly viewed as an intracellular Ca(2+) store. In the last few years the mechanisms regulating the homeostasis of Ca(2+) in the GA and its role in membrane trafficking have begun to be elucidated. Here, these recent discoveries that shed light on the role Ca(2+) plays as of trigger of different steps during membrane trafficking has been reviewed. This includes recruitment of proteins and SNARE cofactors to the Golgi membranes, which are both fundamental for the membrane remodeling and the regulation of fusion/fission events occurring during the passage of cargo across the GA. I conclude by focusing attention on Ca(2+) homeostasis dysfunctions in the GA and their related pathological implications.