It is known that carcinogenesis induces Mg distribution disturbances which cause Mg mobilization through blood cells and Mg depletion in non-neoplastic tissues. Mg deficiency seems to be carcinogenic in cases of some particular haemolymphoreticular diseases only, more often, in cases of solid tumors, it inhibits carcinogenesis. Both carcinogenesis and Mg deficiency increase the plasma membrane permeability and fluidity. The regulation of Mg cellular and subcellular distribution is very important in cancer research. If the Mg level is normal in histones, and particularly in H1 and in nucleic acids on the N7 site of the guanine, it can protect against carcinogenesis. On the other hand, if it is abnormally high it can generate the left-handed Z DNA which is correlated with carcinogenesis. The carcinogenic action of Mg may be linked with some effects on sulfur amino-acid metabolism, growth and the immune system. Although Mg antagonizes certain carcinogenic metals, this is not one of its general properties. Our studies on human amniotic membranes show that Mg acts as a competitive antagonist on 2 or 3 weak carcinogens, Pb and Cd, but not on Co. Mg is a non-competitive antagonist of Ni and is devoid of action on As, both of which are powerful carcinogens. All carcinogenic metals (As, Ni, Cr, Cd, Co, Pb, except Be) reduce the total conductance (Gt). Reversibly all cocarcinogens increase Gt or do not modify it. However, both anticancer and carcinogenic metals reduce Gt. Thus the main target in the relationship between Mg and metals in carcinogenesis is either membrane as regards Pb and Cd, or nucleus as regards Pt, Ga, Co and Ni. The ideal treatment of Mg disturbances in carcinogenesis should control the factors which regulate cellular and subcellular Mg distribution in neoplastic tissues as well as those which avoid Mg depletion in extra malignant tissues.