The purpose of this review is to summarize experimental findings showing that Mg modulates cellular events involved in inflammation. Severe experimental Mg deficiency in the rat induces after a few days a clinical inflammatory syndrome characterized by PMN and macrophage activation, release of inflammatory cytokines and acute phase proteins, excessive production of free radicals. Increasing Mg concentration decreases inflammatory response while reduction in the extracellular Mg results in cell activation. Because Mg acts as a natural calcium antagonist, the molecular basis for inflammatory response is probably the result of modulation of intracellular calcium concentration. Mg deficiency contributes to an exaggerated response to immune stress, hyperlipemia, atherosclerosis, endothelial dysfunction, thrombosis, hypertension and free radical damages. Moreover activated endothelium facilitates adhesion and migration of cancer cells. Experimental findings in animal models suggest that inflammation is the missing link to explain the role of Mg in many pathological conditions.