Both epigenetic and mutagenic events influence the process of carcinogenesis. Any mutagenic event irreversibly alters the genomic information of the cell. Epigenetic activities of compounds do not damage genes directly, but they can alter the gene expression. The most important consequences include alteration of cell proliferation, differentiation, or apoptosis. One of them, which apparently link to the promotion of carcinogenesis is the inhibition of gap-junctional intercellular communication (GJIC) in vitro. These gap junctions allow ions and low-molecular-weight molecules to move between coupled cells, thereby facilitating synchronization of electrotonic or metabolic cooperation. Transient down-regulation by endogenous or exogenous chemicals can bring about adaptive or maladaptive consequences depending on circumstances. Tumor promotors (e.g. DDT) and growth factors reduce GJIC, whereas anticarcinogens and growth inhibitors (e.g., flavonoids, resveratrole, carotenoids) enhance GJIC. Prevention of inhibition of GJIC could be an important chemopreventive strategy of cancer therapy.