Magnesium is the second most abundant intracellular cation in the human body. It serves as a cofactor in over 300 enzymatic reactions and has a profound influence on many cellular processes including DNA and protein synthesis, intracellular signal transduction, and cell growth and differentiation. Not surprisingly, evidence is accumulating that magnesium deficiency contributes to the pathogenesis of a number of human disease states such as atherosclerosis, hypertension, diabetes, and asthma. However, the mechanisms underlying magnesium’s role in various pathological processes remain largely undefined. To begin to elucidate these mechanisms, CodeLink Bioarrays were used to compare liver gene expression profiles of mice maintained on a control diet to those fed a magnesium deficient diet for 3, 7, or 14 days. Magnesium deficiency resulted in the differential expression of a wide variety of genes including several involved in lipid metabolism. This is especially interesting in light of the fact that magnesium is known to modulate blood lipid levels and has been implicated in cardiovascular disease, in particular, atherosclerosis. Genes implicated in diabetes were also differentially expressed. Data such as these should lead to a better understanding and appreciation of magnesium’s role in health and disease.