Studies exploring magnesium deficiency have revealed intricate proinflammatory mechanisms involving calcium and N-methyl-D-aspartate pathways, which elevate proinflammatory cytokines, stimulate reactive oxygen species in endothelial cells and leukocytes, and amplify the release of inflammatory cytokines and acute-phase proteins such as C-reactive protein (CRP) [7,23,24]. This evidence concerns the gene CRP and magnesium deficiency.