Staphylococcus aureus, an opportunistic pathogen present in the nasal cavities of approximatively 25% of the healthy population, causes thousands of deaths per year in the United States alone. This bacterium supports hundreds of millimolar of magnesium (up to 770mM), a concentration much higher than many other bacteria. To maintain intracellular magnesium concentrations within a physiological range bacteria make use of active importers and probably exporters. Here, we study the magnesium homeostasis in Staphylococcus aureus and more precisely the roles of the putative magnesium transporters: mpfA, mpfB, corA1, corA2 and mgtE. We focus mainly on the mutations that appeared to compensate the magnesium sensitivity due to the loss of MpfA, a putative magnesium exporter. We also investigate the question of which importer(s) is/are fundamental for the growth and show that magnesium import in S. aureus relies on the dual activity of both CorA2 and MgtE.